25
10.1 Endocrine Glands (p. 207) Define a hormone, and state the function of hormones. Discuss the difference in mode of action between peptide and steroid hormones. Name the major endocrine glands, and identify their locations. Discuss the control of glandular secretion by nervous mechanisms, hormonal mechanisms, and negative feedback. 10.2 Hypothalamus and Pituitary Gland (p. 211) Explain the anatomical and functional relationships between the hypothalamus and the pituitary gland. Name and discuss two hormones produced by the hypothalamus that are secreted by the posterior pituitary. Name the hormones produced by the anterior pituitary, and indicate which of these control other endocrine glands. 10.3 Thyroid and Parathyroid Glands (p. 214) Discuss the anatomy of the thyroid gland, and the chemistry and physiological function of its hormones. Discuss the function of parathyroid hormone. 10.4 Adrenal Glands (p. 216) Describe the anatomy of the adrenal glands. Discuss the function of the adrenal medulla and its relationship to the nervous system. Name three categories of hormones produced by the adrenal cortex, give an example of each category, and discuss their actions. 10.5 Pancreas (p. 220) Describe the anatomy of the pancreas. Name two hormones produced by the pancreas, and discuss their functions. Discuss the two types of diabetes mellitus, and contrast hypoglycemia with hyperglycemia. 10.6 Other Endocrine Glands (p. 223) Name the most important male and female sex hormones. Discuss their functions. Discuss atrial natriuretic hormone, growth factors, and prostaglandins as hormones not produced by glands. State the location and function of the pineal gland and the thymus gland. 10.7 The Importance of Chemical Signals (p. 226) Give examples to show that chemical signals can act between organs, cells, and individuals. 10.8 Effects of Aging (p. 226) Discuss the anatomical and physiological changes that occur in the endocrine system as we age. 10.9 Homeostasis (p. 226) Discuss how the endocrine system works with other systems of the body to maintain homeostasis. Visual Focus The Hypothalamus and the Pituitary (p. 212) I.C.E—In Case of Emergency Insulin Shock and Diabetic Ketoacidosis (p. 221) What’s New Options For Type I Diabetics: Insulin Pills and More (p. 222) Medical Focus Side Effects of Anabolic Steroids (p. 224) Human Systems Work Together Endocrine System (p. 227) Chapter Outline & Learning Objectives After you have studied this chapter, you should be able to: The Endocrine System 10 John F. Kennedy, the youngest man to be elected president, appeared healthy, vigorous, and active throughout his entire political career. Photos of the president showed a handsome, tanned sailor at the family estate in Massachusetts; others showed the Kennedy family playing football. However, throughout Kennedy’s entire political life, he and his staff took great pains to hide his many ailments—in particular, the fact that Kennedy suffered from Addison’s disease. This rare illness is caused by a deficiency of adrenal cortex hormones, and you can read about it on page 217. (Ironically, one symptom of Addison’s disease is skin that looks like JFK’s signature suntan.) Although he was hospitalized many times, Kennedy repeatedly denied having the disease or any other serious health problems. Yet, medical records tell a different story—the president was in almost constant pain, in part because his vertebrae had been destroyed by the medication for Addison’s disease. At autopsy, his adrenal glands were shrunken and nonfunctional. Still, there is no evidence that Kennedy’s illness affected his performance as president, and he left a legacy that includes the space program and the Peace Corps. C H A P T E R 206

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Page 1: Lon25626 ch10 206-230 - Future is BioTechnology.biotechisfuture.weebly.com/uploads/1/4/1/6/14160671/ch10...10.3 Thyroid and Parathyroid Glands (p.214) • Discuss the anatomy of the

10.1 Endocrine Glands (p.207)

• Define a hormone, and state thefunction of hormones.

• Discuss the difference in mode ofaction between peptide and steroidhormones.

• Name the major endocrine glands, andidentify their locations.

• Discuss the control of glandular secretionby nervous mechanisms, hormonalmechanisms, and negative feedback.

10.2 Hypothalamus and PituitaryGland (p.211)

• Explain the anatomical and functionalrelationships between the hypothalamusand the pituitary gland.

• Name and discuss two hormonesproduced by the hypothalamus that aresecreted by the posterior pituitary.

• Name the hormones produced by theanterior pituitary, and indicate which ofthese control other endocrine glands.

10.3 Thyroid and Parathyroid Glands (p.214)

• Discuss the anatomy of the thyroidgland, and the chemistry andphysiological function of its hormones.

• Discuss the function of parathyroidhormone.

10.4 Adrenal Glands (p.216)

• Describe the anatomy of the adrenalglands.

• Discuss the function of the adrenalmedulla and its relationship to thenervous system.

• Name three categories of hormonesproduced by the adrenal cortex, give anexample of each category, and discusstheir actions.

10.5 Pancreas (p.220)

• Describe the anatomy of the pancreas.

• Name two hormones produced by thepancreas, and discuss their functions.

• Discuss the two types of diabetesmellitus, and contrast hypoglycemiawith hyperglycemia.

10.6 Other Endocrine Glands (p.223)

• Name the most important male andfemale sex hormones. Discuss theirfunctions.

• Discuss atrial natriuretic hormone,growth factors, and prostaglandins ashormones not produced by glands.

• State the location and function of thepineal gland and the thymus gland.

10.7 The Importance of ChemicalSignals (p.226)

• Give examples to show that chemicalsignals can act between organs, cells,and individuals.

10.8 Effects of Aging (p.226)

• Discuss the anatomical andphysiological changes that occur in theendocrine system as we age.

10.9 Homeostasis (p.226)

• Discuss how the endocrine systemworks with other systems of the bodyto maintain homeostasis.

Visual FocusThe Hypothalamus and the Pituitary (p. 212)

I.C.E—In Case of EmergencyInsulin Shock and Diabetic Ketoacidosis (p. 221)

What’s NewOptions For Type I Diabetics: Insulin Pills and More(p. 222)

Medical FocusSide Effects of Anabolic Steroids (p. 224)

Human Systems Work TogetherEndocrine System (p. 227)

Chapter Outline & Learning Objectives After you have studied this chapter, you should be able to:

The Endocrine System

10John F. Kennedy, the youngest man to be elected president, appeared healthy,vigorous, and active throughout his entire political career. Photos of thepresident showed a handsome, tanned sailor at the family estate inMassachusetts; others showed the Kennedy family playing football. However,throughout Kennedy’s entire political life, he and his staff took great pains tohide his many ailments—in particular, the fact that Kennedy suffered fromAddison’s disease. This rare illness is caused by a deficiency of adrenal cortexhormones, and you can read about it on page 217. (Ironically, one symptom ofAddison’s disease is skin that looks like JFK’s signature suntan.) Although hewas hospitalized many times, Kennedy repeatedly denied having the diseaseor any other serious health problems. Yet, medical records tell a differentstory—the president was in almost constant pain, in part because his vertebraehad been destroyed by the medication for Addison’s disease. At autopsy, hisadrenal glands were shrunken and nonfunctional. Still, there is no evidencethat Kennedy’s illness affected his performance as president, and he left alegacy that includes the space program and the Peace Corps.

C H A P T E R

206

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Chapter 10 The Endocrine System 207

10.1 Endocrine Glands

The endocrine system consists of glands and tissues that se-crete hormones. This chapter will give many examples of theclose association between the endocrine and nervous systems.Like the nervous system, the endocrine system is intimatelyinvolved in homeostasis.

Hormones are chemical signals that affect the behavior ofother glands or tissues. Hormones influence the metabolismof cells, the growth and development of body parts, andhomeostasis. Endocrine glands are ductless; they secrete theirhormones directly into tissue fluid. From there, the hormonesdiffuse into the bloodstream for distribution throughout thebody. Endocrine glands can be contrasted with exocrineglands, which have ducts and secrete their products intothese ducts. For example, the salivary glands send saliva intothe mouth by way of the salivary ducts.

Each type of hormone has a unique composition. Evenso, hormones can be categorized as either a peptide hormone(which include proteins, glycoproteins, and modified aminoacids) or a steroid hormone. All steroid hormones are lipidsthat have the same four-carbon ring complex, but each hasdifferent side chains. The majority of hormones are peptides.

Figure 10.1 depicts the locations of the major endocrineglands in the body and Table 10.1 lists the hormones they re-lease. It’s important for you to remember that other organsproduce hormones, too. These additional hormones and theiractions will be described in later chapters. Further, hormonesaren’t the only type of chemical signal. Neurotransmitters(which you learned about in Chapter 9) are one example ofsignaling molecules that allow direct communication fromcell to cell, and you’ll learn about others here as well.

How Hormones Function

Along with fundamental differences in structure, peptide andsteroid hormones also function differently. Most peptidehormones bind to a receptor protein in the plasma mem-brane and activate a “second messenger” system (Fig. 10.2).The “second messenger” causes the cellular changes forwhich the hormone is credited. As an analogy, suppose youare the person in charge of a crew assigned to redecorate aroom. As such, you stand outside the room and direct theworkers inside the room. The workers clean, paint, applywallpaper, etc. Like the “boss” in this analogy, the peptidehormone stays outside the cell and directs activities within.The peptide hormone, or “first messenger,” activates a “sec-ond messenger”—the crew workers inside the cell. Commonsecond messengers found in many body cells include cyclicAMP (made from ATP, and abbreviated cAMP) and calcium.The second messenger sets in motion an enzyme cascade, so-called because each enzyme in turn activates several others,and so on. These intracellular enzymes cause the changes inthe cell that are associated with the hormone. Because of thesecond messenger system, the binding of a single peptidehormone can result in as much as a thousandfold response.

The cellular response can be a change in cellular behavior orthe formation of an end product that leaves the cell. For ex-ample, by activating a second messenger, insulin causes thefacilitated diffusion of glucose into body cells, while thyroid-stimulating hormone causes thyroxine release from the thy-roid gland.

Because steroid hormones are lipids, they diffuse across theplasma membrane and other cellular membranes (Fig. 10.3).Inside the cell, steroid hormones such as estrogen and proges-terone bind to receptor proteins. The hormone-receptor com-plex then binds to DNA, activating particular genes. Activationleads to production of a cellular enzyme in varying quantities.Again, it is largely intracellular enzymes that cause the cellularchanges for which the hormone receives credit. For example, es-trogen directs cellular enzymes that cause the growth of axillaryand pubic hair in an adolescent female.

When protein hormones such as insulin are used formedical purposes, they must be administered by injection. Ifthese hormones were taken orally, they would be acted on bydigestive enzymes. Once digested, insulin cannot carry out itsfunctions. Steroid hormones, such as those in birth controlpills, can be taken orally because they’re water-insolublelipids and poorly digested. Steroids can pass through the di-gestive tract largely undigested, and then diffuse through theplasma membrane into the cell.

Hormone Control

The release of hormones is usually controlled by one or more ofthree mechanisms: (1) the concentration of dissolved moleculesor ions in the blood, referred to as humoral control; (2) by the ac-tions of other hormones; and/or (3) by the nervous system.

It’s important for ions or molecules in the body to be kept within a normal range to maintain homeostasis. Thus,humoral control determines the secretion of many bodyhormones. For example, when the blood glucose level risesfollowing a meal, the pancreas secretes insulin. Insulin causesthe liver to store glucose and the cells to take up glucose, andblood glucose is lowered back to normal. Once the blood glu-cose concentration is corrected, the pancreas stops producinginsulin. In much the same way, a low level of calcium ions inthe blood stimulates secretion of parathyroid hormone (PTH)from the parathyroid gland. When blood calcium rises to anormal level, secretion of PTH stops. These examples of hu-moral control illustrate regulation by negative feedback.

Hormone release can also be controlled by specific stim-ulating or inhibiting hormones. Thyroid-stimulating hor-mone (TSH) from the pituitary gland (also called thyrotropin)does exactly what its name implies—it stimulates the thyroidgland to produce thyroid hormone. By contrast, the release ofinsulin is inhibited by the production of glucagon by the pan-creas. Insulin lowers the blood glucose level, whereasglucagon raises it. In subsequent sections of this chapter,you’ll learn about other instances in which pairs of hormoneswork opposite to one another, and thereby bring about theregulation of a substance in the blood.

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208 PART III Integration and Coordination

Figure 10.1 Anatomical location of major endocrine glands in the body. The hypothalamus and pituitary gland are in the brain, the thyroid and parathyroids are in the neck, and the adrenal glands and pancreas are in the pelvic cavity.The gonads include the ovaries infemales, located in the pelvic cavity, and the testes in males, located outside this cavity in the scrotum. Not shown is the pineal gland, located inthe brain.The thymus gland lies within the thoracic cavity.

parathyroid glands (posterior surface of thyroid)

testis (male)

ovary (female)

PITUITARY GLAND

Posterior Pituitary

Release ADH and oxytocin produced by the hypothalamus

Anterior PituitaryThyroid stimulating (TSH):

stimulates thyroid

Adrenocorticotropic (ACTH): stimulates adrenal cortex

Gonadotropic (FSH, LH): egg and sperm production; sex hormone production

Prolactin (PL): milk production

Growth (GH): bone growth, protein synthesis, and cell division

THYROID GLAND Thyroxine (T4) and triiodothyronine

(T3): increase metabolic rate; regulates growth and development

Calcitonin: lowers blood calcium level

HYPOTHALAMUS

Releasing and inhibiting hormones:regulate the anterior pituitary

Antidiuretic (ADH):water reabsorption by kidneys

Oxytocin: stimulates uterine contraction and milk letdown

ADRENAL GLAND

Adrenal cortexGlucocorticoids (cortisol):

raises blood glucose level; stimulates breakdown of protein

Mineralocorticoids (aldosterone): reabsorption of sodium and excretion of potassium

Sex hormones: reproductive organs and bring about sex characteristics

Adrenal medullaEpinephrine and norepinephrine:

active in emergency situations; raise blood glucose level

GONADS

TestesAndrogens (testosterone):male sex characteristics

OvariesEstrogens and progesterone:female sex characteristics

PARATHYROIDS Parathyroid hormone (PTH):

raises blood calcium level

PANCREASInsulin: lowers blood glucose

level; formation of glycogenGlucagon: increases blood

glucose level; breakdown of glycogen

THYMUS GLAND Thymosins: production and

maturation of T lymphocytes

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Chapter 10 The Endocrine System 209

Hypothalamic-releasing andinhibiting hormones

Antidiuretic (ADH)

Oxytocin

Thyroid-stimulating (TSH)

Adrenocorticotropic (ACTH)

Gonadotropic

Follicle-stimulating (FSH)

Luteinizing (LH)

Prolactin (PRL)

Growth (GH)

Melanocyte-stimulating (MSH)

Thyroxine (T4) and triiodothyronine (T3)

Calcitonin

Parathyroid (PTH)

Glucocorticoids (cortisol)

Mineralocorticoids (aldosterone)

Sex hormones

Epinephrine and norepinephrine

Insulin

Glucagon

Androgens (testosterone)

Estrogens and progesterone

Thymosins

Melatonin

Hypothalamus

Produced byhypothalamus,released fromposterior pituitary

Anterior pituitary

Thyroid

Parathyroids

Adrenal gland

Adrenal cortex

Adrenal medulla

Pancreas

GonadsTestes

Ovaries

Thymus

Pineal gland

TABLE 10.1 Principal Endocrine Glands and Hormones

Endocrine Hormone Chemical Target Chief Function(s)Gland Released Class Tissues/Organs of Hormone

Peptide

Peptide

Peptide

Glycoprotein

Peptide

Glycoprotein

Protein

Protein

Peptide

Iodinated amino acid

Peptide

Peptide

Steroid

Steroid

Steroid

Modified amino acid

Protein

Protein

Steroid

Steroid

Peptide

Modified amino acid

Anterior pituitary

Kidneys

Uterus, mammaryglands

Thyroid

Adrenal cortex

Gonads

Mammary glands

Soft tissues, bones

Melanocytes in skin

All tissues

Bones, kidneys,intestine

Bones, kidneys,intestine

All tissues

Kidneys

Gonads, skin,muscles, bones

Cardiac and othermuscles

Liver, muscles,adipose tissue

Liver, muscles,adipose tissue

Gonads, skin,muscles, bones

Gonads, skin,muscles, bones

T lymphocytes

Brain

Regulate anterior pituitary hormones

Stimulates water reabsorption by kidneys

Stimulates uterine muscle contraction,release of milk by mammary glands

Stimulates thyroid

Stimulates adrenal cortex

Egg and sperm production; sex hormoneproduction

Milk production

Cell division, protein synthesis, and bonegrowth

Unknown function in humans; regulatesskin color in lower vertebrates

Increases metabolic rate; regulates growthand development

Lowers blood calcium level

Raises blood calcium level

Raise blood glucose level; stimulatebreakdown of protein

Reabsorb sodium and excrete potassium

Stimulate reproductive organs and bringabout sex characteristics

Released in emergency situations; raiseblood glucose level

Lowers blood glucose level;promotes formation of glycogen

Raises blood glucose level

Stimulate male sex characteristics

Stimulate female sex characteristics

Stimulate production and maturation of T lymphocytes

Controls circadian and circannual rhythms;possibly involved in maturation of sexualorgans

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The nervous system is an important controller of the en-docrine system. Upon receiving sensory information fromthe body, the brain can make appropriate adjustments tohormone secretion to ensure homeostasis. For example,while you eat a meal, sensory information is relayed to thebrain. In turn, the brain signals parasympathetic motor neu-rons to release insulin from the pancreas. (Recall that theparasympathetic neurons control “rest and digest” func-tions.) Insulin will allow body cells to take up glucose fromdigested food.

It’s important to stress that many hormones are influ-enced by more than one control mechanism. In the previous

examples, you can see that insulin release is influenced by allthree controllers: humoral, hormonal, and neural control.For the majority of hormones, control is regulated by nega-tive feedback. As you know from Chapter 1, in a negativefeedback system, a stimulus causes a body response. Thebody response, in turn, corrects the initial stimulus. The re-sult is that the activity of the hormone is maintained withinnormal limits and homeostasis is ensured. However, in a fewinstances, positive feedback controls the release of ahormone—for example, release of oxytocin during labor anddelivery (discussed on page 211).

210 PART III Integration and Coordination

Figure 10.3 Action of a steroid hormone. A steroid hormoneresults in a hormone-receptor complex that activates DNA andprotein synthesis.

ATP

cAMP(second messenger)

capillary

peptide hormone (first messenger)

receptor protein

plasma membrane

activated enzyme

1. Hormone binds to a receptor in the plasma membrane.

2. Binding leads to activation of an enzyme that changes ATP to cAMP.

3. cAMP activates an enzyme cascade.

4. Many molecules of glycogen are broken down to glucose, which enters the bloodstream.

glycogen

glucose (leaves cell and goes to blood)

Figure 10.2 Action of a peptide hormone. The binding of apeptide hormone leads to cAMP and then to activation of anenzyme cascade. In this example, the hormone causes glycogen tobe broken down to glucose.

steroid hormone

plasma membrane

1. Hormone diffuses through plasma membrane because it is lipid soluble.

2. Hormone binds to receptor inside nucleus.

3. Hormone-receptor complex activates gene and synthesis of a specific mRNA molecule follows.

4. mRNA moves to ribosomes, and protein synthesis occurs.

receptor protein DNA

mRNA

mRNA

ribosome

protein

nucleus

cytoplasm

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Chapter 10 The Endocrine System 211

Content CHECK-UP!

1. Antidiuretic hormone (ADH), a peptide hormone, works by:

a. binding to a receptor outside the cell and activating a secondmessenger.

b. diffusing into the cell, binding to a receptor inside the cell, andactivating a second messenger.

c. diffusing into the cell, binding to a receptor inside the cell, andactivating genes in DNA.

2. Testosterone, a steroid hormone, works by:

a. binding to a receptor outside the cell and activating a secondmessenger.

b. diffusing into the cell, binding to a receptor inside the cell, andactivating a second messenger.

c. diffusing into the cell, binding to a receptor inside the cell, andactivating genes in DNA.

3. Antidiuretic hormone stimulates the kidneys to reabsorb water and return it to the blood plasma. ADH release is controlled by anegative feedback system.Which action causes ADH to be released?

a. drinking a big bottle of water

b. finishing a marathon race and becoming dehydrated

Answers in Appendix C, page 463.

10.2 Hypothalamus and Pituitary Gland

The hypothalamus regulates the internal environment. Forexample, through the autonomic system, the hypothalamushelps control heartbeat, body temperature, and water balance(by creating thirst). The hypothalamus also controls the glan-dular secretions of the pituitary gland (hypophysis). Thepituitary, a small gland about 1 cm in diameter, is connectedto the hypothalamus by a stalklike structure. The pituitary hastwo portions: the posterior pituitary (neurohypophysis)and the anterior pituitary (adrenohypophysis).

Posterior Pituitary

Neurons in the hypothalamus called neurosecretory cells pro-duce the hormones antidiuretic hormone (ADH) and oxytocin(Fig. 10.4, left). These hormones pass through axons into theposterior pituitary (neurohypophysis) where they are stored inaxon endings. Thus, the hypothalamic hormones antidiuretichormone and oxytocin are produced in the hypothalamus, butare released into the bloodstream from the posterior pituitary.

Antidiuretic Hormone and Oxytocin

Certain neurons in the hypothalamus are sensitive to the water-salt balance of the blood. When these cells determine that theblood is too concentrated, antidiuretic hormone (ADH, alsocalled vasopressin) is released from the posterior pituitary. In yourbody, blood becomes concentrated if you have just finished exer-cising heavily and body water has been lost as sweat. Upon reach-ing the kidneys, ADH causes more water to be reabsorbed intokidney capillaries. As the blood becomes dilute once again, ADH

is no longer released. This is an example of control by negativefeedback because the effect of the hormone (to dilute blood) actsto shut down the release of the hormone. An additional effect ofADH is to raise blood pressure, by vasoconstriction of blood ves-sels throughout the body (hence, the hormone’s additionalname of vasopressin). This mechanism also illustrates negativefeedback: Blood pressure falls because body water is lost as sweat(stimulus); vasopressin is released (response); blood vessels con-strict and blood pressure rises to normal (stimulus corrected).Negative feedback maintains stable conditions and homeostasis.

Inability to produce ADH causes diabetes insipidus(watery urine), in which a person produces copious amountsof urine with a resultant loss of ions from the blood. The con-dition can be corrected by the administration of ADH.

It’s interesting to note that alcohol suppresses ADH pro-duction and release. When ADH is absent, the kidneys don’treabsorb as much water. The person drinking alcohol urinatesmore often and may become dehydrated as a result. Thesymptoms of the drinker’s “hangover”—headache, nausea,dizziness—are largely due to dehydration.

Oxytocin, the other hormone made in the hypothalamus,causes uterine contraction during childbirth and milk letdownwhen a baby is nursing. The more the uterus contracts during la-bor, the more nerve impulses reach the hypothalamus, causingoxytocin to be released. Similarly, the more a baby suckles, themore oxytocin is released. In both instances, the release of oxy-tocin from the posterior pituitary is controlled by positive feed-back—that is, the stimulus continues to bring about an effect thatever increases in intensity. Positive feedback is not the best way tomaintain stable conditions and homeostasis. However, it worksduring childbirth and nursing because external mechanisms in-terrupt the process. In childbirth, the delivery of the baby and af-terbirth (the placenta and membranes surrounding the baby)eventually stops oxytocin secretion. When a baby with a fulltummy stops nursing, that, too, halts oxytocin secretion. For anursing mother, the letdown response to oxytocin becomes auto-matic over time. Thus, it is referred to as a neuroendocrine reflex.Whenthebabybeginstosuckle, thepressureandtouchsensationssignal the hypothalamus, oxytocin is released, and the stream ofbreast milk begins. Similarly, hearing a baby cry—even someoneelse’s baby—will cause a nursing mother’s breast milk to flow.

Anterior Pituitary

A portal system lies between the hypothalamus and the ante-rior pituitary (Fig. 10.4, center). In this example, the term portalsystem is used to describe the following unique pattern ofcirculation:

capillaries y vein y capillaries y vein

The hypothalamus controls the anterior pituitary by produc-ing hypothalamic-releasing hormones and hypothalamic-inhibiting hormones. For example, there is a thyrotropin-releasing hormone (TRH) and a prolactin-inhibitinghormone (PIH). TRH stimulates the anterior pituitary to se-crete thyroid-stimulating hormone, and PIH inhibits the pitu-itary from secreting prolactin.

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212 PART III Integration and Coordination

1. Neurosecretory cells produce ADH and oxytocin.

2. These hormones move down axons to axon terminals.

3. When appropriate, ADH and oxytocin are secreted from axon terminals into the bloodstream.

1. Neurosecretory cells produce hypothalamic-releasing and hypothalamic-inhibiting hormones.

2. These hormones are secreted into a portal system.

3. Each type of hypothalamic hormone either stimulates or inhibits production and secretion of an anterior pituitary hormone.

4. The anterior pituitary secretes its hormones into the bloodstream, which delivers them to specific cells, tissues, and glands.

hypothalamus

optic chiasm

Posterior pituitary Anterior pituitary

portal system

Thyroid: thyroid-stimulating hormone (TSH)

Adrenal cortex:

adrenocorticotropic hormone (ACTH)

Mammary glands: prolactin (PRL)

Bones, tissues: growth hormone (GH)

Ovaries, testes: gonadotropic hormones (FSH, LH)

Kidney tubules and

blood vessels: antidiuretichormone (ADH)

Smooth muscle

in uterus: oxytocin

Mammary glands: oxytocin

Figure 10.4 The hypothalamus and the pituitary. Left: The hypothalamus produces two hormones, ADH and oxytocin, which are stored andsecreted by the posterior pituitary. Right: The hypothalamus controls the secretions of the anterior pituitary, and the anterior pituitary controls thesecretions of the thyroid, adrenal cortex, and gonads, which are also endocrine glands. It also secretes growth hormone and prolactin.

Visual Focus

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Chapter 10 The Endocrine System 213

Hormones That Affect Other Glands

Four of the hormones produced by the anterior pituitary havean effect on other glands: Thyroid-stimulating hormone(TSH) stimulates the thyroid to produce the thyroid hormones;adrenocorticotropic hormone (ACTH) stimulates the adrenalcortex to produce its hormones; and gonadotropic hor-mones (follicle-stimulating hormone—FSH and luteinizinghormone—LH) stimulate the gonads—the testes in males andthe ovaries in females—to produce gametes and sex hormones.The hypothalamus, the anterior pituitary, and other glandscontrolled by the anterior pituitary are all involved in self-regulating negative feedback mechanisms that maintain stableconditions. In each instance, the blood level of the last hormonein the sequence exerts negative feedback control over the secre-tion of the first two hormones:

greatest during childhood and adolescence, when most bodygrowth is occurring (Fig. 10.5). If too little GH is producedduring childhood, the individual has pituitary dwarfism,characterized by perfect proportions but small stature. If toomuch GH is secreted, a person can become a giant (Fig. 10.5).Giants usually have poor health, primarily because GH has asecondary effect on the blood sugar level, promoting anillness called diabetes mellitus (see page 220).

On occasion, GH is overproduced in the adult and a condi-tion called acromegaly results. Because long bone growth is nolonger possible in adults, the feet, hands, and face (particularlythe chin, nose, and eyebrow ridges) can respond, and these por-tions of the body become overly large (Fig. 10.6).

?Begin Thinking ClinicallyAn adenoma, which is one type of pituitary glandtumor, can affect the production of one or morepituitary hormones. What would be the effect ofa prolactin adenoma in a man?Answer and discussion in Appendix C, page 463.

Effects of Growth Hormone

The amount of GH produced by the anterior pituitary affectsthe height of the individual. The quantity of GH produced is

Content CHECK-UP!

4. Name three anterior pituitary hormones that cause the release ofanother hormone(s).

5. Oxytocin release from the hypothalamus during labor anddelivery is a mechanism that works by:

a. positive feedback. b. negative feedback.

6. Which of the following is an effect of growth hormone?

a. It promotes fat metabolism.

b. It stimulates protein synthesisin bone and cartilage.

Figure 10.5 Effect of growth hormone. The amount of growthhormone produced by the anterior pituitary during childhoodaffects the height of an individual.Too much growth hormone canlead to giantism, while an insufficient amount results in limitedstature and even pituitary dwarfism.

Feedback inhibitsrelease of hormone 1

Feedback inhibitsrelease of hormone 2

releasing hormone(hormone 1)

Hypothalamus

Anterior pituitary

Target gland

stimulating hormone(hormone 2)

target gland hormone(hormone 3)

Effects of Other Hormones

Other hormones produced by the anterior pituitary do notaffect other endocrine glands. Prolactin (PRL) is producedbeginning at about the fifth month of pregnancy, and is pro-duced in quantity after childbirth. It causes the mammaryglands in the breasts to develop and produce milk. It alsoplays a role in carbohydrate and fat metabolism.

Growth hormone (GH), or somatotropic hormone,stimulates protein synthesis within cartilage, bone, and mus-cle. It stimulates the rate at which amino acids enter cells andprotein synthesis occurs. It also promotes fat metabolism asopposed to glucose metabolism.

c. It causes a person togrow taller.

d. all of the above

Answers in Appendix C, page 463.

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10.3 Thyroid and Parathyroid Glands

The thyroid gland is a large gland located in the neck, whereit is attached to the trachea just below the larynx (see Fig.10.1). The parathyroid glands are embedded in the posteriorsurface of the thyroid gland.

Thyroid Gland

The thyroid gland is composed of a large number of follicles,each a small spherical structure made of thyroid cells filledwith triiodothyronine (T3), which contains three iodineatoms, and thyroxine (T4), which contains four iodineatoms. These are the two forms of thyroid hormone; T3 isthought to have the greatest effect on the body.

Effects of Thyroid Hormones

To produce triiodothyronine and thyroxine, the thyroid glandactively acquires iodine. The concentration of iodine in thethyroid gland can increase to as much as 25 times that of theblood. If iodine is lacking in the diet, the thyroid gland isunable to produce the thyroid hormones. In response toconstant stimulation by the anterior pituitary, the thyroid en-larges, resulting in a simple, or endemic, goiter (Fig. 10.7).Some years ago, it was discovered that the use of iodized saltallows the thyroid to produce the thyroid hormones, andtherefore helps prevent simple goiter.

Thyroid hormones increase the metabolic rate. They donot have a single target organ; instead, they stimulate all cellsof the body to metabolize at a faster rate. More glucose is bro-ken down, and more energy is utilized.

If the thyroid fails to develop properly, a condition calledcongenital hypothyroidism results (Fig. 10.8). Individuals

with this condition are short and stocky and have had ex-treme hypothyroidism (undersecretion of thyroid hormone)since infancy or childhood. Thyroid hormone therapy can ini-tiate growth, but unless treatment is begun within the firsttwo months of life, severe developmental delay results. Theoccurrence of hypothyroidism in adults produces the condi-tion known as myxedema, which is characterized by lethargy,weight gain, loss of hair, slower pulse rate, lowered body

214 PART III Integration and Coordination

Figure 10.6 Acromegaly. Acromegaly is caused by overproduction of GH in the adult. It is characterized by enlargement of the bones in theface, the fingers, and the toes as a person ages.

Age 9 Age 16 Age 33 Age 52

Figure 10.7 Simple goiter. An enlarged thyroid gland is oftencaused by a lack of iodine in the diet.Without iodine, the thyroid isunable to produce its hormones, and continued anterior pituitarystimulation causes the gland to enlarge.

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Chapter 10 The Endocrine System 215

temperature, and thickness and puffiness of the skin. Theadministration of adequate doses of thyroid hormonesrestores normal function and appearance.

In the case of hyperthyroidism (oversecretion of thyroidhormone), as seen in Graves’ disease, the thyroid gland isoveractive, and a goiter forms. This type of goiter is calledexophthalmic goiter. The eyes protrude because of edema ineye socket tissues and swelling of the muscles that move theeyes. The patient usually becomes hyperactive, nervous, and ir-ritable, and suffers from insomnia. Removal or destruction ofa portion of the thyroid by means of radioactive iodine is gen-erally effective in curing the condition. Hyperthyroidism canalso be caused by a thyroid tumor, which is usually detected asa lump during physical examination. Again, the treatment issurgery in combination with administration of radioactiveiodine. The prognosis for most patients is excellent.

Calcitonin

Calcium (Ca2�) plays a significant role in both nervous con-duction and muscle contraction. It is also necessary for coag-ulation (clotting) of blood. The blood calcium level is regulatedin part by calcitonin, a hormone secreted by the thyroidgland when the blood calcium level rises (Fig. 10.9). The pri-mary effect of calcitonin is to bring about the deposit of cal-cium in the bones. It does this by temporarily reducing theactivity and number of osteoclasts. Recall from Chapter 6 thatthese cells break down bone. When the blood calcium lowersto normal, the release of calcitonin by the thyroid is inhibited,but a low calcium level stimulates the release of parathyroid

Figure 10.9 Regulation of blood calcium level. Top: When theblood calcium (Ca2�) level is high, the thyroid gland secretescalcitonin. Calcitonin promotes the uptake of Ca2� by the bones, andtherefore the blood Ca2� level returns to normal. Bottom: When theblood Ca2� level is low, the parathyroid glands release parathyroidhormone (PTH). PTH causes the bones to release Ca2�. It also causesthe kidneys to reabsorb Ca2� and activate vitamin D; thereafter, theintestines absorb Ca2�.Therefore, the blood Ca2� level returns tonormal.

Figure 10.8 Congenital hypothyroidism. Individuals who havehypothyroidism since infancy or childhood do not grow and developas others do. Unless medical treatment is begun, the body is shortand stocky. Developmental delay is also likely.

high blood Ca2+

low blood Ca2+

Thyroid gland secretes calcitonin into blood. Bones

take up Ca2+

from blood.

Blood Ca2+

lowers.

Blood Ca2+

rises.

Intestines absorb Ca2+

from digestive tract.

Kidneys reabsorb Ca2+

from kidney tubules.

Bones release Ca2+

into blood.

parathyroid hormone (PTH)

Parathyroid glands

release PTHinto blood.

activated vitamin D

calcitonin

Homeostasis (normal blood Ca2+)

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hormone (PTH) by the parathyroid glands. Calcitonin is animportant hormone in children, whose skeleton is undergo-ing rapid growth. It is of minor importance in adults. Parathy-roid hormone is the major controller of calcium homeostasis.However, calcitonin can be used therapeutically in adults toreduce the effects of osteoporosis (see the Medical Focus onpage 102).

Parathyroid Glands

Parathyroid hormone (PTH), the hormone produced bythe parathyroid glands, causes the blood phosphate(HPO4

2�) level to decrease and the ionic blood calcium(Ca2�) level to increase. The antagonistic actions of calci-tonin, from the thyroid gland, and parathyroid hormone,from the parathyroid glands, maintain the blood calciumlevel within normal limits.

Note in Figure 10.9 that after a low blood calcium levelstimulates the release of PTH, it promotes release of calciumfrom the bones. (It does this by promoting the activity of os-teoclasts.) PTH promotes the reabsorption of calcium by thekidneys, where it also activates vitamin D. Vitamin D, in turn,stimulates the absorption of calcium from the intestine. Theseeffects bring the blood calcium level back to the normal rangeso that the parathyroid glands no longer secrete PTH.

Many years ago, the four parathyroid glands were some-times mistakenly removed during thyroid surgery because oftheir size and location in the thyroid. When insufficientparathyroid hormone production leads to a dramatic drop inthe blood calcium level, hypocalcemic tetany results. Intetany, the body shakes from continuous muscle contraction.This effect is brought about by increased excitability of thenerves, which initiate nerve impulses spontaneously andwithout rest. In severe cases, hypocalcemic tetany is fatal.

10.4 Adrenal Glands

The adrenal glands sit atop the kidneys (see Fig. 10.1). Eachadrenal gland consists of an inner portion called the adre-nal medulla and an outer portion called the adrenal cor-tex. These portions, like the anterior pituitary and the pos-terior pituitary, have no physiological connection with oneanother. The adrenal medulla is under nervous control, andthe adrenal cortex is under the control of ACTH (also calledcorticotropin), an anterior pituitary hormone. Stress ofall types, including emotional and physical trauma,prompts the hypothalamus to stimulate the adrenal glands(Fig. 10.10).

Adrenal Medulla

The hypothalamus initiates nerve impulses that travel by wayof the brain stem, spinal cord, and sympathetic nerve fibers tothe adrenal medulla, which then secretes its hormones.

Epinephrine (adrenaline) and norepinephrine (nora-drenaline) produced by the adrenal medulla rapidly bringabout all the body changes that occur when an individual re-acts to an emergency situation. The release of epinephrineand norepinephrine achieves the same results as sympatheticstimulation—the “fight-or-flight” responses: increased heartrate, rapid respiration, dilation of the pupils, etc. Thus, thesehormones assist sympathetic nerves in providing a short-termresponse to stress.

Adrenal Cortex

There are three layers in the adrenal cortex, and each producesa different set of steroid hormones. The hormones producedby the adrenal cortex provide a long-term response to stress(Fig. 10.10). The two major types of hormones produced bythe adrenal cortex are the mineralocorticoids and the gluco-corticoids. The mineralocorticoids regulate salt and waterbalance, leading to increases in blood volume and blood pres-sure. The glucocorticoids regulate carbohydrate, protein, andfat metabolism, leading to an increase in blood glucose level.Cortisone, the medication often administered for inflamma-tion of joints, is a glucocorticoid.

The adrenal cortex also secretes small amounts of bothmale and female sex hormones—regardless of one’s gender.Both male and female sex hormones promote skeletal growthin adolescents. The male hormones from the adrenal glandstimulate the growth of axillary and pubic hair at puberty. Inaddition, male hormones help to sustain the sex drive, orlibido, in both men and women.

Glucocorticoids

Cortisol is a biologically significant glucocorticoid producedby the adrenal cortex. Cortisol raises the blood glucose levelin at least two ways: (1) It promotes the breakdown of mus-cle proteins to amino acids, which are taken up by the liverfrom the bloodstream. The liver then converts these excess

216 PART III Integration and Coordination

Content CHECK-UP!

7. Which of the following conditions is caused by excessive thyroidhormone?

a. Graves’ disease

b. cretinism (congenital hypothyroidism)

c. simple goiter

d. myxedema

8. Which mineral is necessary to manufacture thyroid hormones?

a. sodium c. calcium

b. iron d. iodine

9. The target organs for parathyroid hormone are:

a. kidney, liver, stomach.

b. kidney, bone, liver.

c. kidney, bone, small intestine.

d. bone, liver, small intestine.

Answers in Appendix C, page 463.

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Chapter 10 The Endocrine System 217

amino acids to glucose, which enters the blood. (2) Cortisolpromotes the metabolism of fatty acids rather than carbohy-drates, and this spares glucose for the brain.

Glucocorticoid Therapy

Cortisol and other forms of glucocorticoids suppress thebody’s normal reaction to disease—the inflammatory reac-tion (see Fig. 13.4) and the immune process. Cortisone is theglucocorticoid that is used as a medication. Because it reducesinflammation, cortisone reduces swelling and pain in jointdisorders such as tendonitis and osteoarthritis. Clinicians alsotreat automimmune disorders, such as rheumatoid arthritis,organ transplant rejection, allergies, and severe asthma bysuppressing the immune response with cortisone therapy.However, cortisone should be used for the minimum timepossible because long-term administration for therapeuticpurposes causes some degree of Cushing’s syndrome (seepage 218). Further, impaired immunity resulting from corti-sone use predisposes the individual to infection and in-

creased cancer risk. In addition, sudden withdrawal from cor-tisone therapy causes symptoms of diminished secretory ac-tivity by the adrenal cortex. This occurs because cortisonemedication suppresses the release of adrenocorticotropic hor-mone (ACTH) by the anterior pituitary, leading to a decreasein natural glucocorticoid production by the adrenal cortex.Therefore, withdrawal of cortisone following long-term usemust be tapered. During an alternate-day schedule, thedosage is gradually reduced and then finally discontinued asthe patient’s adrenal cortex resumes activity.

Mineralocorticoids

Aldosterone is the most important of the mineralocorticoids.Aldosterone primarily targets the kidney where it promotesrenal absorption of sodium (Na�) and water, and renal excre-tion of potassium (K�).

As one might expect, secretion of mineralocorticoidsfrom the adrenal cortex is influenced by ACTH (adrenocorti-cotropic hormone or corticotropin) from the pituitary

epinephrine

spinal cord (cross section)

norepinephrine

sympathetic fibers

neuron cell body

adrenal medulla

path of nerve impulses

hypothalamus

Heartbeat and blood pressure increase. Blood glucose level rises. Muscles become energized.

Stress Response:

Short Term

neurosecretory cells produce hypothalamic-releasing hormones

anterior pituitary secretes ACTH

adrenal cortex

ACTH

Protein and fat metabolisminstead of carbohydrate breakdown.

Reduction of inflammation;immune cells are suppressed.

Sodium ions and water are reabsorbed by kidney. Blood volume and pressure increase.

Stress Response:

Long Term

Glucocorticoids

Mineralocorticoids

stress

glucocorticoids

mineralocorticoids

Figure 10.10 Adrenal glands. Both the adrenal medulla and the adrenal cortex are under the control of the hypothalamus when they helpus respond to stress. Left: The adrenal medulla provides a rapid, but short-term stress response. Right: The adrenal cortex provides a slower, butlong-term stress response.

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gland. However, the pituitary hormone is not the primarycontroller for aldosterone secretion. When the bloodsodium level and therefore the blood pressure are low, thekidneys secrete renin (Fig. 10.11). Renin is an enzyme thatconverts the plasma protein angiotensinogen to angiotensinI. Angiotensin I is fully activated to angiotensin II by a con-verting enzyme found in lung capillaries. Angiotensin IIstimulates the adrenal cortex to release aldosterone. The ef-fect of this system, called the renin-angiotensin-aldosteronesystem, is to raise blood pressure in two ways: Angiotensin IIconstricts arterioles, and aldosterone causes the kidneys toreabsorb sodium. When the blood sodium level rises, wateris reabsorbed, in part because the hypothalamus secretesADH (see page 211). Reabsorption means that water enterskidney capillaries and thus returns to the blood. Then bloodpressure increases to normal.

There is an antagonistic hormone to aldosterone, as youmight suspect. When the atria of the heart are stretched due toincreased blood volume, cardiac cells release a hormonecalled atrial natriuretic hormone (ANH, or atriopeptide),which inhibits the secretion of aldosterone from the adrenalcortex. The effect of ANH is the excretion of sodium—that is,natriuresis. When sodium is excreted, so is water, and thereforeblood pressure lowers to normal.

Malfunction of the Adrenal Cortex

Malfunction of the adrenal cortex can lead to a syndrome, aset of symptoms that occur together. The syndromes com-monly associated with the adrenal cortex are Addison’s diseaseand Cushing’s syndrome.

Addison’s Disease and Cushing’s Syndrome

When the level of adrenal cortex hormones is low due to hy-posecretion, a person develops Addison’s disease. The pres-ence of excessive but ineffective ACTH causes a bronzing ofthe skin because ACTH can lead to a buildup of melanin(Fig. 10.12). Without cortisol, glucose cannot be replenishedwhen a stressful situation arises. Even a mild infection canlead to death. The lack of aldosterone results in a loss ofsodium and water, the development of low blood pressure,and possibly severe dehydration. Left untreated, Addison’sdisease can be fatal.

When the level of adrenal cortex hormones is high dueto hypersecretion, a person develops Cushing’s syndrome(Fig. 10.13). The excess cortisol results in a tendency towarddiabetes mellitus as muscle protein is metabolized and sub-cutaneous fat is deposited in the midsection. The trunk isobese, while the arms and legs remain a normal size. An ex-cess of aldosterone and reabsorption of sodium and waterby the kidneys leads to a basic blood pH and hypertension.The face is moon-shaped due to edema. Masculinizationmay occur in women because of excess adrenal male sexhormones.

218 PART III Integration and Coordination

Figure 10.11 Regulation of blood pressure and volume.

Bottom: When the blood sodium (Na�) level is low, low bloodpressure causes the kidneys to secrete renin. Renin leads to thesecretion of aldosterone from the adrenal cortex. Aldosterone causesthe kidneys to reabsorb Na�, and water follows, so that bloodvolume and pressure return to normal. Top: When the blood Na� ishigh, a high blood volume causes the heart to secrete atrialnatriuretic hormone (ANH). ANH causes the kidneys to excrete Na�,and water follows.The blood volume and pressure return to normal.

Heart secretes atrial natriuretic hormone (ANH)

into blood.

Kidneys extrete Na+ and water

in urine.

Blood pressure drops.

renin

Kidneys secrete renin into blood.

atrial natriuretic hormone (ANH)

Blood pressure rises.

angiotensin I and II aldosterone

Kidneys reabsorb Na+

and water from kidney tubules.

Adrenal cortex secretes

aldosterone into blood.

Homeostasis (normal blood pressure)

high blood Na+

low blood Na+

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Chapter 10 The Endocrine System 219

Content CHECK-UP!

10. From the following list of hormones of the adrenal cortex and theircorresponding effects, choose the pair, or pairs, that are correct.

a. male hormones → stimulate sex drive

b. aldosterone → increases sodium concentration in the blood

c. female hormones → promote long bone growth in adolescents

d. pairs b and c are correct.

e. all are correct.

11. Which hormone opposes the effect of aldosterone in thebody?

a. renin

b. angiotensin I

c. atrial natriuretic hormone

d. cortisol

12. Aldosterone returns blood pressure to normal by causing thekidneys to reabsorb water and sodium. Because it works by anegative feedback mechanism, which of the following actionscould cause aldosterone to be released?

a. giving a unit of blood

b. drinking a big bottle of a sports drink

c. running a marathon and becoming dehydrated

d. both a and c are correct

Answers in Appendix C, page 463.

Figure 10.13 Cushing’s syndrome.

Cushing’s syndrome results fromhypersecretion of adrenal cortex hormones.a. Patient first diagnosed with Cushing’ssyndrome. b. Four months later, after therapy.

a. b.

Figure 10.12 Addison’s disease. Addison’s disease is characterized by a peculiar bronzing of the skin, particularly noticeable in these light-skinned individuals. Note the color of (a) the face and (b) the hands compared to the hand of an individual without the disease.

b.a.

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10.5 Pancreas

The pancreas is a long organ that lies transversely in the ab-domen between the kidneys and near the duodenum of thesmall intestine. It is composed of two types of tissue. Ex-ocrine tissue produces and secretes digestive juices that go byway of ducts to the small intestine. Endocrine tissue, calledthe pancreatic islets (islets of Langerhans), produces and se-cretes the hormones insulin and glucagon directly into theblood (Fig. 10.14).

The two antagonistic hormones, insulin and glucagon,both produced by the pancreas, help maintain the normallevel of glucose in the blood. Insulin is secreted when theblood glucose level is high, which usually occurs just aftereating. Insulin stimulates the uptake of glucose by mostbody cells. Insulin is not necessary for the transport of glu-cose into brain or red blood cells, but muscle cells and adi-pose tissue cells require insulin for glucose transport. In liverand muscle cells, insulin stimulates enzymes that promotethe storage of glucose as glycogen. In muscle cells, the glu-cose supplies energy for muscle contraction, and in fat cells,glucose enters the metabolic pool and thereby supplies glyc-erol for the formation of fat. In these ways, insulin lowersthe blood glucose level.

Glucagon is secreted from the pancreas, usually betweenmeals, when the blood glucose level is low. The major targettissues of glucagon are the liver and adipose tissue. Glucagonstimulates the liver to break down glycogen to glucose andto use fat and protein in preference to glucose as energysources. Adipose tissue cells break down fat to glycerol andfatty acids. The liver takes these up and uses them as sub-strates for glucose formation. In these ways, glucagon raisesthe blood glucose level.

Diabetes Mellitus

Diabetes mellitus is a fairly common hormonal disease inwhich insulin-sensitive body cells are unable to take upand/or metabolize glucose. Therefore, the blood glucoselevel is elevated—a condition called hyperglycemia. Be-cause body cells cannot access glucose, starvation occurs atthe cell level. The person becomes extremely hungry—acondition called polyphagia. As the blood glucose levelrises, glucose will be lost in the urine (glycosuria). Glucosein the urine causes excessive water loss through urination(polyuria). The loss of water in this way causes the diabeticto be extremely thirsty (polydipsia). Glucose is not beingmetabolized, so the body turns to the breakdown of proteinand fat for energy. Fat metabolism leads to the buildup ofketones in the blood, and excretion of ketones in the urine(ketonuria). Because ketones are acidic, their buildup inthe blood causes acidosis (acid blood), which can lead tocoma and death.

We now know that diabetes mellitus exists in twoforms. In type I, more often called insulin-dependent dia-

220 PART III Integration and Coordination

Figure 10.14 Regulation of blood glucose level. Top: When theblood glucose level is high, the pancreas secretes insulin. Insulinpromotes the storage of glucose as glycogen in the liver andmuscles and the use of glucose to form fat in adipose tissue.Therefore, insulin lowers the blood glucose level. Bottom: When theblood glucose level is low, the pancreas secretes glucagon. Glucagonacts opposite to insulin; therefore, glucagon raises the blood glucoselevel to normal.

high blood glucose

low blood glucose

After eating, pancreas

secretes insulin into blood.

Liver stores glucose from

blood as glycogen.

Glucose level drops.

insulin

Glucose level rises.

Muscle cells store glycogen

and build protein.

Adipose tissue uses glucose from blood to

form fat.

Between eating, pancreas secretes

glucagon into blood.

glucagon

Liver breaks down glycogen

to glucose. Glucose enters

blood.

Adipose tissue breaks down fat.

Homeostasis (normal blood glucose)

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Chapter 10 The Endocrine System 221

betes mellitus (IDDM), the pancreas does not produce in-sulin. This condition is believed to be brought on, at least inpart, by exposure to an environmental agent. This agent—very likely a virus—causes an extreme immune response,and immune cells destroy the pancreatic islets. As a result,the individual must have daily insulin injections. Daily in-jections control the diabetic symptoms, but diabetics canstill experience life-threatening problems, as described inI.C.E. box above.

Of the 16 million people who now have diabetes in theUnited States, most have type II, more often called noninsulin-dependent diabetes (NIDDM). This type of diabetes mel-litus usually occurs in people of any age who tend to beobese. Researchers theorize that perhaps adipose tissueproduces a substance that interferes with the transport of

glucose into cells. The amount of insulin in the blood ofthese patients is normal or elevated, but the insulin recep-tors on the cells do not respond to it. It is possible to pre-vent, or at least control, type II diabetes by adhering to alow-fat, low-sugar diet, maintaining a healthy weight, andexercising regularly. If these attempts fail, oral drugs areavailable to stimulate the pancreas to secrete more insulin.Other oral medications enhance the metabolism of glu-cose in the liver and muscle cells. It is projected that asmany as 7 million Americans may have type II diabeteswithout being aware of it. Yet, the effects of untreated typeII diabetes are as serious as those of type I diabetes. In addition, without stringent control the NIDDM diabeticwill ultimately require insulin injections, thus becominginsulin-dependent.

mone that raises blood glucose. If the blood glucose isn’t too

low, the insulin shock can be corrected at home. However, one

should never attempt to give food or drinks to someone who is

semiconscious or unconscious—she could easily choke. Instead,

the inside of her cheeks can be smeared with glucose gel,

honey, syrup, or frosting, which will melt and be swallowed. If

the patient doesn’t quickly become alert enough to eat or drink,

she must be transported to an emergency room. There, an injec-

tion of glucagon or an intravenous solution will quickly raise the

blood glucose level.

Diabetic ketoacidosis is caused by blood glucose that is too

high. It commonly results when the diabetic eats a meal, but for-

gets to inject insulin. Infection, injury, or extreme stress can also

lead to DKA. The symptoms of DKA are increased thirst, frequent

urination, nausea, and vomiting. The patient breathes rapidly, and

his breath smells like fruit-flavored gum. His pulse is very fast, but

his blood pressure is low. Without an identifying bracelet or tag, he

could easily be mistaken as someone who’s had too much to drink:

sluggish, lethargic, and increasingly sleepy. If untreated, he’ll

eventually fall into a diabetic coma. Fortunately, under a physi-

cian’s direction, a trained paramedic can start an intravenous solu-

tion to help dilute the patient’s blood. As he is being transported to

the emergency room, EMS personnel can then measure the glucose

and ketones in his blood to provide a complete history, in prepara-

tion for more complete treatment in the hospital.

If you’re someone with diabetes mellitus, the disorder involving

the hormone insulin, you already know the importance of main-

taining a stable blood glucose level to ensure your long-term

health. If your roommate, friend, or loved one is a diabetic, you

need to be informed too, because a diabetic’s possible prob-

lems don’t always take a long time to develop. Insulin shock

and diabetic ketoacidosis (DKA) can develop very rapidly, and

both can be fatal or result in permanent brain damage. It’s im-

portant for diabetics and their friends and family to recognize

the symptoms of insulin shock and DKA, and know how to use a

glucometer to measure blood glucose and how to give an

injection.

Insulin shock (also called an insulin reaction) results when

blood glucose falls to critically low levels—a condition called

hypoglycemia. It often results when the diabetic patient acci-

dentally injects too much insulin, or takes her insulin but

misses a meal. The patient is likely to feel anxious, sweat pro-

fusely, and complain of a headache. She may become hyperac-

tive, confused, and even psychotic as the condition worsens.

Eventually, she’ll lose consciousness and lapse into a so-called

diabetic coma.

It’s critical for first responders to try to raise the patient’s

blood glucose as quickly as possible. If she is conscious and

alert, she can quickly drink milk, juice, or soda, or eat something

sweet. She may be able to self-inject with glucagon, the hor-

Insulin Shock and Diabetic Ketoacidosis

I.C.E. — IN CASE OF EMERGENCY

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222 PART III Integration and Coordination

insulin. New research has refined the combination of anti-rejection drugs, and more transplanted cells now survive. Now,fewer than 300,000 cells are needed, and the large majority ofresearch participants no longer require insulin injections. Cur-rently, both animal and living human donor cells are being in-vestigated as potential sources for the large quantities of isletcells used for transplant (Fig. 10A). Investigators are also look-ing for ways to entirely eliminate the need for anti-rejectiondrugs. At present, all transplant patients must have lifelonganti-rejection medications, which have severe side effects (re-curring infections, increased cancer risk, kidney damage, etc.).A technique called microencapsulation shields donor cells frombeing rejected by enclosing them in tiny membrane capsules. Ifthese studies are successful, patients won’t need anti-rejectionmedication or insulin injections. Researchers are optimisticthat microencapsulated islet cells might soon be available fortransplant.

“I can remember getting sick with the flu when I was 11. I missedtwo or three days of school, and I just never got my strength back.I ate and drank constantly because I was thirsty and hungry all thetime. I was always in the bathroom, and I started wetting the bed—can you imagine, at age 11? I fell asleep in school, and the teachercould barely get me to wake up. That’s when my doctor diagnosedmy diabetes for the first time.”

The patient, age 25, is a typical type I, juvenile-onset, orinsulin-dependent, diabetic. Her symptoms are typical of insulin-dependent diabetes mellitus (IDDM) (see pages 220–221). Asyou know, in insulin-dependent diabetes, the body’s own im-mune cells destroy the islet cells. To treat their illness, type Idiabetic patients must inject insulin three or more times daily oruse an insulin pump device continuously. Patients use bloodtests to check their blood glucose levels. Further, diabetics mustalso monitor their diet, activity, and stress levels. Regular exer-cise is also a must.

To provide treatment options that are less painful, and po-tentially more effective and reliable, researchers are actively ex-ploring alternative delivery systems for obtaining insulin with-out injections. Scientists at the University of Texas at Austinhave recently published research on an insulin pill. Currently,diabetics can’t swallow their insulin because harsh stomachacid destroys the protein, digesting it before it can be ab-sorbed. A newly developed gel that can be used in pill formsuccessfully shields the insulin as it passes through the stom-ach. The gel then attaches to the wall of the intestine, allowinginsulin to be successfully taken into the bloodstream. In addi-tion, skin patches and insulin aerosol sprays are already inclinical trials on human patients. Successful development ofthese products could help diabetics maintain stable levels ofblood glucose, eliminate injections, and lead more normallives.

Pancreatic islet cell transplantation shows great promise asa permanent cure for type I diabetes. Unlike a whole pancreatictransplant, which is major surgery, islet cell transplant is a rela-tively simple procedure. The cells are first harvested from a ca-daver pancreas, then directly injected into the liver where theyform colonies and produce insulin. Initially, an islet cell trans-plant required approximately 700,000 cells to produce enough

Options for Type I Diabetics Insulin Pills and More

Figure 10 A Encapsulated insulin-producing pancreatic isletcells from pigs can be transplanted into patients without theneed for immune system-suppressing drugs.

Long-term complications of both types of diabetes areblindness, kidney disease, and circulatory disorders, includ-ing atherosclerosis, heart disease, stroke, and reduced circula-tion. The latter can lead to gangrene in the arms and legs.Pregnancy carries an increased risk of diabetic coma, and the

child of a diabetic is somewhat more likely to be stillborn orto die shortly after birth. However, these complications of di-abetes are not expected to appear if the mother’s blood glu-cose level is carefully regulated and kept within normal limitsduring the pregnancy.

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Chapter 10 The Endocrine System 223

Content CHECK-UP!

13. Insulin-sensitive cells in the human body include:

a. muscle cells. d. a and b.

b. adipose tissue cells. e. all of the above.

c. brain and nerve cells.

14. Which of the following is an effect of glucagon?

a. causes the liver to break down stored glycogen

b. causes adipose tissue to store fat

c. lowers blood glucose level

d. stimulates the liver to store glucose as glycogen

15. Glucagon release is controlled by a negative feedback system.Which action causes glucagon to be released?

a. skipping breakfast and going to morning classes with anempty stomach

b. eating a big holiday meal

c. running a marathon race for several hours without pausing for food

d. a and c

e. b and c

Answers in Appendix C, page 463.

10.6 Other Endocrine Glands

The body has a number of other endocrine glands, includingthe gonads (testes in males and the ovaries in females).Other lesser-known glands, such as the thymus gland andthe pineal gland, also produce hormones. Some tissueswithin organs produce hormones and/or growth factors. In-dividual body cells produce local messenger chemicalstermed prostaglandins.

Testes and Ovaries

The testes are located in the scrotum, and the ovaries are lo-cated in the pelvic cavity. The testes produce androgens (e.g.,testosterone), which are the male sex hormones, and theovaries produce estrogens and progesterone, the female sexhormones. The hypothalamus and the pituitary gland controlthe hormonal secretions of these organs in the manner previ-ously described on page 212.

Androgens

Puberty is the time of life when sexual maturation occurs.Greatly increased testosterone secretion during puberty stim-ulates the growth of the penis and the testes. Testosteronealso brings about and maintains the male secondary sex char-acteristics that develop during puberty, including the growthof a beard, axillary (underarm) hair, and pubic hair. Itprompts the larynx and the vocal cords to enlarge, causingthe voice to change. It is partially responsible for the muscu-lar strength of males. This is why some athletes take supple-

mental amounts of anabolic steroids, which are eithertestosterone or related chemicals. The contraindications oftaking anabolic steroids are discussed in the Medical Focuson page 224. Testosterone also stimulates oil and sweatglands in the skin; therefore, it is largely responsible for acneand body odor. Another side effect of testosterone is bald-ness. Genes for baldness are probably inherited by bothsexes, but baldness is seen more often in males because of thepresence of testosterone.

Estrogen and Progesterone

The female sex hormones, estrogens and progesterone, havemany effects on the body. In particular, estrogens secretedduring puberty stimulate the growth of the uterus and thevagina. Estrogen is necessary for ovum maturation and islargely responsible for the secondary sex characteristics in fe-males, including female body hair and fat distribution. Ingeneral, females have a more rounded appearance than malesbecause of a greater accumulation of fat beneath the skin.Also, the pelvic girdle is wider in females than in males, re-sulting in a larger pelvic cavity. Both estrogen and proges-terone are required for breast development and for regulationof the uterine cycle, which includes monthly menstruation(discharge of blood and mucosal tissues from the uterus).

Thymus Gland

The lobular thymus gland, which lies just beneath the ster-num (see Fig. 10.1), reaches its largest size and is most activeduring childhood. Lymphocytes are white blood cells thatoriginate in the bone marrow and are responsible for specificdefenses against a particular invader. When lymphocytescomplete development in the thymus, they are transformedinto thymus-derived lymphocytes, or T lymphocytes. Thelobules of the thymus are lined by epithelial cells that secretehormones called thymosins. These hormones aid in the dif-ferentiation of lymphocytes packed inside the lobules.Although the hormones secreted by the thymus ordinarilywork only in the thymus, researchers hope that these hor-mones could be injected into AIDS or cancer patients wherethey would enhance T-lymphocyte function.

Pineal Gland

The pineal gland, which is located in the brain, produces thehormone melatonin, primarily at night. Melatonin is in-volved in our daily sleep-wake cycle; normally we grow sleepyat night when melatonin levels increase and awaken oncedaylight returns and melatonin levels are low (Fig. 10.15).Daily 24-hour cycles such as this are called circadian rhythms.Circadian rhythms are controlled by an internal timing mech-anism called a biological clock.

Based on animal research, it appears that melatonin alsoregulates sexual development. It has also been noted that chil-dren whose pineal gland has been destroyed due to a braintumor experience early puberty.

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Hormones from Other Tissues

We have already mentioned that the heart produces atrial na-triuretic hormone (see page 218). The kidney also influencescardiovascular system function by producing the hormone ery-thropoietin (EPO), which stimulates red blood cell produc-tion by the bone marrow. And you will see in Chapter 15 thatorgans and tissues of the digestive system produce hormonesas well.

Leptin

Leptin is a protein hormone produced by adipose tissue. Lep-tin acts on the hypothalamus, where it signals satiety—thatthe individual has had enough to eat. Strange to say, theblood of obese individuals may be rich in leptin. It is possiblethat the leptin they produce is ineffective because of a geneticmutation, or else their hypothalamic cells lack a suitablenumber of receptors for leptin.

224 PART III Integration and Coordination

winter

summer

6 P.M.

a.

b.

c.

6 A.M.

winter

summer

Figure 10.15 Melatonin production. Melatonin production isgreatest at night when we are sleeping. Light suppresses melatoninproduction (a) so its duration is longer in the winter (b) than in thesummer (c).

They’re called “performance-enhancing steroids,” and their use is al-leged to be widespread in athletics, both amateur and professional.Whether the sport is baseball, football, professional cycling, or trackand field events, no activity seems to be safe from drug abuse. Re-cent steroid abuse admitted by Marion Jones has forever changedOlympic history. Jones was the first female athlete to win fivemedals for track and field events during the 2000 Sydney Olympics.In 2008, she was stripped of all medals she had earned, as well asdisqualified from a fifth-place finish in the 2004 Athens games. Fu-ture Olympic record books will not include her name, and therecords of her teammates in the relay events have also been tainted.

Baseball records will also likely require revisions. The ex-citing slugfest between Mark McGwire and Sammy Sosa in thesummer of 1998 was largely credited with reviving national in-terest in baseball. Yet, the great home-run competition drewunwanted attention to the darker side of professional sports,when it was alleged that both McGwire and Sosa were both us-ing anabolic steroids at the time. Similar charges of drug abusemay prevent baseball great Roger Clemens from entering theBaseball Hall of Fame, despite his record for the number of CyYoung awards he holds. Likewise, because controversy contin-ues to surround baseball legend Barry Bonds, this talented ath-lete may never achieve Hall of Fame status. Although he scoreda record 715 home runs and won more Most Valuable Playerawards than anyone in history, Bonds remains accused ofsteroid abuse. Lou Canseco of the Oakland Athletics and JasonGiambi of the New York Yankees have both admitted usingperformance-enhancing drugs.

Side Effects of Anabolic Steroids

Most athletes and officials continue to deny use of anabolicsteroids in professional sports. However, many people from bothinside and outside the industry maintain that such abuse hasbeen going on for many years, and that it continues despite thenegative publicity. Congress continues to investigate the contro-versy, yet the finger-pointing and accusations increase. Oftremendous concern to lawmakers, educators, and parents is theincreased use of steroids by teens wishing to bulk up quickly,perhaps seeking to be just like the sports figures they admire.

Anabolic steroids are synthetic forms of the male sex hormonetestosterone. Taking doses 10 to 100 times the amount prescribed bydoctors for various illnesses promotes larger muscles when the per-son also exercises. Trainers may have been the first to acquire ana-bolic steroids for weight lifters, bodybuilders, and other athletes,such as professional baseball players. However, being a steroid usercan have serious detrimental effects. Men often experience de-creased sperm counts and decreased sexual desire due to atrophy ofthe testicles. Some develop an enlarged prostate gland or growbreasts. On the other hand, women can develop male sexual charac-teristics. They grow hair on their chests and faces, and lose hair fromtheir heads; many experience abnormal enlargement of the clitoris.Some cease ovulating or menstruating, sometimes permanently.

Some researchers predict that two or three months of high-dosage use of anabolic steroids as a teen can cause death by age 30 or40. Steroids have even been linked to heart disease in both sexes andimplicated in the deaths of young athletes from liver cancer and onetype of kidney tumor. Steroids can cause the body to retain fluid,which results in increased blood pressure. Users then try to get rid of

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Chapter 10 The Endocrine System 225

Growth Factors

A number of different types of organs and cells produce pep-tide growth factors, which stimulate cell division and mitosis.Some, such as lymphokines, are released into the blood; oth-ers diffuse to nearby cells. Growth factors of particular interestare the following:

Granulocyte and macrophage colony-stimulating factor (GM-CSF) is secreted by many different tissues. GM-CSFcauses bone marrow stem cells to form eithergranulocyte or macrophage cells (both are forms ofwhite blood cells, or leukocytes), depending on whetherthe concentration is low or high.

Platelet-derived growth factor is released from platelets andfrom many other cell types. It helps in wound healingand causes an increase in the number of fibroblasts,

smooth muscle cells, and certain cells of the nervoussystem.

Epidermal growth factor and nerve growth factor stimulate thecells indicated by their names, as well as many others.These growth factors are also important in woundhealing.

Tumor angiogenesis factor stimulates the formation ofcapillary networks and is released by tumor cells. Onetreatment for cancer is to prevent the activity of thisgrowth factor.

Prostaglandins

Prostaglandins are potent chemical signals produced withincells from arachidonate, a fatty acid. Prostaglandins are notdistributed in the blood; instead, they act locally, quite close

“steroid bloat” by taking largedoses of diuretics. A youngCalifornia weight lifter had afatal heart attack after usingsteroids, and the postmortemshowed a lack of electrolytes,salts that help regulate theheart. Finally, steroid abusehas psychological effects, in-cluding depression, hostility,aggression, and eating disor-ders. Unfortunately, thesedrugs make a person feel in-vincible. One abuser even hadhis friend videotape him as hedrove his car at 40 miles anhour into a tree!

The many harmful ef-fects of anabolic steroids aregiven in Figure 10B. The Fed-eral Food and Drug Adminis-tration now bans moststeroids, and steroid use hasalso been banned by the National Collegiate AthleticAssociation (NCAA), theNational Football League(NFL), and the InternationalOlympic Committee (IOC).

'roid mania– hostility and aggression; delusions and hallucinations; depression upon withdrawal

balding in men and women;hair on face and chestin women

beard and deepening of voice in women

kidney disease andretention of fluids,called "steroid bloat"

breast enlargementin men and breastreduction in women

severe acne

high blood cholesteroland atherosclerosis;high blood pressureand damage to heart

liver dysfunctionand cancer

in women, increased sizeof ovaries; cessation of ovulation and menstruation

stunted growth in youngstersby prematurely halting activity of the epiphyseal plates

reduced testicular size, low sperm count, and impotency

Figure 10 B The effects of anabolic steroid use.

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226 PART III Integration and Coordination

to where they were produced. In the uterus, prostaglandinscause muscles to contract and may be involved in the painand discomfort of menstruation. Also, prostaglandins medi-ate the effects of pyrogens, chemicals that are believed to resetthe temperature regulatory center in the brain. For example,aspirin reduces body temperature and controls pain becauseof its effect on prostaglandins.

Certain prostaglandins reduce gastric secretion andhave been used to treat ulcers; others lower blood pressureand have been used to treat hypertension; and still othersinhibit platelet aggregation and have been used to preventthrombosis (the formation of stationary clots in bloodvessels). However, different prostaglandins have contraryeffects, and it has been very difficult to successfully stan-dardize their use.

Content CHECK-UP!

16. From the following list of endocrine glands and their hormones,choose the pair that is correct:

a. ovaries → androgens c. kidney → aldosterone

b. thymus → insulin d. adipose tissue → leptin

17. Which of the following is a local tissue messenger that stimulatesnearby cells?

a. leptin c. melatonin

b. prostaglandin d. thymosin

18. Describe three functions of the female sex hormones.

Answers in Appendix C, page 463.

10.7 The Importance of Chemical Signals

Chemical signals are molecules that affect the behavior ofthose cells that have receptor proteins to receive them. For ex-ample, a hormone that binds to a receptor protein affects themetabolism of the cell. Cells, organs, and even individualscommunicate with one another by using chemical signals.

We are most familiar with chemical signals that are pro-duced by organs some distance from one another in the body.For example, hormones produced by the anterior pituitary in-fluence the function of numerous organs throughout thebody. Insulin, produced by the pancreas, is transported inblood to muscle, adipose, and other insulin-sensitive cells.The nervous system at times utilizes chemical signals that areproduced by an organ distant from the one being affected, aswhen the hypothalamus produces releasing hormones. Asyou know, these releasing hormones then travel in a portalsystem to the anterior pituitary gland.

Many chemical signals act locally—that is, from cell tocell. Prostaglandins are local hormones, and certain neurotrans-mitter substances released by one neuron affect a neuronnearby. Growth factors, which fall into this category, are veryimportant regulators of cell division. Some growth factors arebeing used as medicines to promote the production of bloodcells in AIDS and cancer patients. When a tumor develops, cell

division occurs even when no detectable stimulatory growthfactor has been received. And the tumor produces a growth fac-tor called tumor angiogenesis factor, which promotes theformation of capillary networks to service its cells.

Chemical Signals Between Individuals

Chemical signals that act between individuals are calledpheromones. Pheromones are well exemplified in other ani-mals, but they may also be effective between people. Humansproduce airborne chemicals from a variety of areas, includingthe scalp, oral cavity, armpits, genital areas, and feet. For ex-ample, the armpit secretions of one woman could possibly af-fect the menstrual cycle of another woman. Women who livein the same household often have menstrual cycles in syn-chrony. Also, the cycle length becomes more normal whenwomen with irregular cycles are exposed to extracts of malearmpit secretions.

10.8 Effects of Aging

Thyroid disorders and diabetes are the most significant en-docrine problems affecting health and function as we age.Both hypothyroidism and hyperthyroidism are seen in theelderly. Graves’ disease is an autoimmune disease that targetsthe thyroid, resulting in symptoms of cardiovascular disease,increased body temperature, and fatigue. In addition, a pa-tient may experience weight loss of as much as 20 pounds, de-pression, and mental confusion. Hypothyroidism (myxedema)may fail to be diagnosed because the symptoms of hair loss,skin changes, and mental deterioration are attributed simplyto the process of aging.

The true incidence of IDDM diabetes among the elderly isunknown. Its symptoms can be confused with those of othermedical conditions that are present. As in all adults, NIDDMdiabetes is associated with being overweight and often can becontrolled by proper diet.

The effect of age on the sex organs is discussed inChapter 17.

10.9 Homeostasis

The endocrine system and the nervous system work togetherto regulate the organs of the body and thereby maintainhomeostasis. It is clear from reviewing the Human SystemsWork Together illustration on page 227 that the endocrinesystem particularly influences the digestive, cardiovascular,and urinary systems in a way that maintains homeostasis.

The endocrine system helps regulate digestion. The digestivesystem adds nutrients to the blood, and hormones producedby the digestive system influence the gallbladder and pancreasto send their secretions to the digestive tract. Another hormone,gastrin, promotes the digestion of protein by the stomach.Through its influence on the digestive process, the endocrinesystem promotes the presence of nutrients in the blood.

The endocrine system helps regulate fuel metabolism. Control-ling the level of glucose in the blood is the function of insulin

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Chapter 10 The Endocrine System 227

ale)

us

ovart

y

eas

als

s

Androgens activate sebaceous glands andhelp regulate hair growth.

Skin provides sensoryinput that results in theactivation of certainendocrine glands.

Growth hormone regulatesbone development; para-thyroid hormone and calcitonin regulate Ca2+

content.

Bones provide protectionfor glands; store Ca2+ usedas second messenger.

Skeletal System

Growth harmone andandrogens promote growthof skeletal muscle;epinephrine stimulatesheart and constricts bloodvessels.

Muscles help protectglands.

Muscular System

Sex hormones affectdevelopment of brain.

Nervous System

Hypothalamus is part ofendocrine system; nervesinnervate glands of secretion.

Epinephrine increases bloodpressure; ADH, aldosterone,and atrial natriuretichormone help regulateblood volume; growth factorscontrol blood cell formation.

Blood vessels transporthormones from glands;blood services glands; heartproduces atrial natriuretichormones.

Cardiovascular System

Epinephrine promotesventilation by dilatingbronchioles; growth factorscontrol production of redblood cells that carryoxygen.

Respiratory System

Gas exchange in lungsprovides oxygen and ridsbody of carbon dioxide.

Hormones help controlsecretion of digestive glands and accessoryorgans; insulin andglucagon regulate glucosestorage in liver.

Digestive System

Stomach and small intes-tine produce hormones.

ADH, aldosterone, andatrial natriuretic hormoneregulate reabsorption ofwater and Na+ by kidneys.

Urinary System

Kidneys keep blood valueswithin normal limits so thattransport of hormonescontinues.

Hypothalamic, pituitary,and sex hormones controlsex characteristics andregulate reproductiveprocesses.

Reproductive System

Gonads produce sexhormones.

Thymus is necessaryfor maturity ofT lymphocytes.

Lymphatic System/Immunity

Lymphatic vessels pick upexcess tissue fluid;immune system protectsagainst infections.

How the EndocrineSystem works with otherbody systems.

Integumentary System

Human Systems Work Together ENDOCRINE SYSTEM

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228 PART III Integration and Coordination

SELECTED NEW TERMSBasic Key Terms

adrenal cortex (uh-dre’nul kor’teks), p. 216

adrenal gland (uh-dre’nul gland), p. 216

adrenal medulla (uh-dre’nul me -dul’uh), p. 216

adrenocorticotropic hormone (uh-dre’no-kor”ti-ko -tro p’ik hor’mon), p. 212

aldosterone (al”dos’ter-on), p. 217

anabolic steroid (an”uh-bol’ik ste’royd), p. 223

androgen (an’dro-jen), p. 223

anterior pituitary (an-ter’e-or pı-tu’ ı-tar”e), p. 211

antidiuretic hormone (an”tı-dı”y u-ret’ikhor’mon), p. 211

atrial natriuretic hormone (a’tr e-al na”tre-yu-ret’ik hor’mon), p. 218

atriopeptide (a-tre-yo-pep-tıd), p. 218

calcitonin (kal”sı-to’nin), p. 215

circadian rhythm (ser”ka’de-an r ı’thm), p. 223

corticotropin (kor’tı-ko-troh-pın), p. 216

cortisol (kor’tı-sol), p. 216

cyclic AMP (sik’lik AMP), p. 207

endocrine gland (en’do-krin gland), p. 207

epinephrine (ep” ı-nef ’rin), p. 216

estrogen (es’tro-jen), p. 223

glucagon (glu’kuh-gon), p. 220

glucocorticoid (glu’ko-kor’tı-koyd), p. 216

gonad (go’nad), p. 223

gonadotropic hormone (go”nad-o-trop’ikhor’mon), p. 213

prostaglandins (pros”tuh-glan’dinz), p. 225

renin (re’nin), p. 218

steroid hormone (steer’oyd hor’mon), p. 207

testis (tes’tis), p. 223

testosterone (tes-tos’te-ron), p. 223

thymosin (thi’mo-sin), p. 223

thymus gland (thi’mus gland), p. 223

thyroid gland (thi’royd gland), p. 214

thyroid-stimulating hormone (thi’roydstim’yu-lat-ing hor’mon), p. 212

thyrotropin (thı’ro-tro-’pın), p. 207

thyroxine (thı-rok’sin), p. 214

Clinical Key Terms

acidosis (as’ı-do’sıs), p. 220

acromegaly (ak”ro-meg’uh-le), p. 213

Addison’s disease (a’dı-sons dı-zez’), p. 218

congenital hypothyroidism (kon-gen’i-tulhi”po-thi’-roy-dizm), p. 214

Cushing’s syndrome (koosh’ings sin’drom), p. 218

diabetic coma (dı”uh-be tik ko�-muh), p. 221

diabetes insipidus (dı”uh-be’teez in-sipı-dus),p. 211

diabetic ketoacidosis (dı”uh-be tik ke’ to�-as-i-do�sus), p. 221

exophthalmic goiter (ek”sof-thal’mik goy’ter),p. 215

glycosuria (gli’ko-sur’e-uh), p. 220

Graves’ disease (gravz dı-zeez’), p. 215

growth factor (groth fak’tor), p. 224

growth hormone (groth hor’mon), p. 213

hormone (hor’mon), p. 207

hypothalamic-inhibiting hormone (hi”po-the-lam’ik-in-hib’it-ing hor’mon), p. 211

hypothalamic-releasing hormone (hi”po-the-lam’ik-re-les’-ing hor’mon), p. 211

hypothalamus (hi’po-thal’ -m s), p. 211

insulin (in’suh-lin), p. 220

leptin (lep’tin), p. 224

melatonin (mel”uh-to’nin), p. 223

mineralocorticoids (min”er-al-o-kor’tı-koyds),p. 216

norepinephrine (nôr’eep-neef ’rın), p. 216

ovary (o’var-e), p. 223

oxytocin (ok”si-to’sin), p. 211

pancreas (pan’kre-us), p. 220

pancreatic islets (of Langerhans) (pan”kre-at’ikı’lets ov lahng’er-hanz), p. 220

parathyroid gland (par”uh-thi’royd gland), p. 216

parathyroid hormone (par”uh-thi’royd hor’mon), p. 216

peptide hormone (pep’tid hor’mon), p. 207

pineal gland (pin’e-ul gland), p. 223

pituitary gland (pı-tu’ ı-tar”e gland), p. 211

portal system (por’tul sis’ tem), p. 211

posterior pituitary (pos-ter’e-or pı-tu’-ı-tar”e),p. 211

progesterone (pro-jes’ter- on), p. 223

prolactin (pro-lak’tin), p. 213

ee

and glucagon. Just after eating, insulin encourages the uptake ofglucose by cells and the storage of glucose as glycogen in the liverand muscles. In between eating, glucagon stimulates the liver tobreak down glycogen to glucose so that the blood glucose levelstays constant. Adrenaline (epinephrine) from the adrenalmedulla also stimulates the liver to release glucose. Glucagon(from the pancreas) and cortisol (from the adrenal cortex) pro-mote the breakdown of protein to amino acids, which can beconverted to glucose by the liver. They also promote the metab-olism of fatty acids to conserve glucose, a process called glucosesparing. Finally, the thyroid hormones thyroxine and tri-iodothyronine set the body’s metabolic rate, and thus are thehormones that ultimately regulate fuel metabolism.

The endocrine system helps regulate blood pressure and vol-ume. ADH produced by the hypothalamus (but secreted bythe posterior pituitary) promotes reabsorption of water by thekidneys, especially when we have not been drinking waterthat day. Aldosterone produced by the adrenal cortex causesthe kidneys to reabsorb sodium, and when the level ofsodium rises, water is automatically reabsorbed so that bloodvolume and pressure rise. Regulation by the endocrine systemoften involves antagonistic hormones; in this case, ANH (atri-opeptide) produced by the heart causes sodium excretion.

The endocrine system helps regulate calcium balance. Theconcentration of calcium (Ca2�) in the blood is critical be-cause this ion is important to nervous conduction, musclecontraction, and the action of hormones. As you know fromstudying Chapter 6, the bones serve as a reservoir for cal-cium. When the blood calcium concentration lowers,parathyroid hormone promotes the breakdown of bone andthe reabsorption of calcium by the kidneys, and the absorp-tion of calcium by the intestines. Opposing the action ofparathyroid hormone, calcitonin secreted by the thyroidbrings about the deposit of calcium in the bones (althoughthis function of calcitonin is more important in growingchildren than in adults).

The endocrine system helps regulate response to the externalenvironment. In “fight-or-flight” situations, the nervous sys-tem stimulates the adrenal medulla to release epinephrine(adrenaline), which has a powerful effect on various or-gans. This, too, is important to homeostasis because it al-lows us to behave in a way that keeps us alive. Any damagedue to stress is then repaired by the action of other hor-mones, including cortisol. Glucocorticoid (e.g., cortisone)therapy is useful for its antiinflammatory and immunosup-pressive effects.

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Chapter 10 The Endocrine System 229

hyperglycemia (hi”per-gli-se’me-uh), p. 220

hypoglycemia (hi”po-gli-se’me-uh), p. 221

insulin-dependent diabetes mellitus (in’sul-in-de-pen’dent di”uh-be’teez mee-li’tus), p. 220

insulin shock (in�sul-in shok), p. 221

ketonuria (ke”to-nu’re-uh), p. 220

polyphagia (pol”e-fa-je-uh), p. 220

polyuria (pol”e-yu-re-uh), p. 220

simple (endemic) goiter (sim’pl en-dem’ıkgoy’ter), p. 214

syndrome (sin’drom), p. 218

tetany (tet’uh-ne), p. 216

myxedema (mik”se-de’muh), p. 214

noninsulin-dependent diabetes (non’in’sul-in-de-pen’dent di”uh-bee’tez), p. 221

pituitary dwarfism (pı-tuı-tar”e dwarf ’-izm), p. 213

polydipsia (pol”e-dip’se-uh), p. 220

SUMMARY10.1 Endocrine Glands

A. Endocrine glands secretehormones into the bloodstream,and from there they are distributedto target organs or tissues.

B. Hormones are either peptides orsteroids. Reception of a peptidehormone at the plasma membraneactivates an enzyme cascade insidethe cell. Steroid hormonescombine with a receptor in the cell,and the complex attaches to andactivates DNA. Protein synthesisfollows. The major endocrineglands and hormones are listed inTable 10.1. Neural mechanisms,hormonal mechanisms, and/ornegative feedback control theeffects of hormones.

10.2 Hypothalamus and Pituitary GlandA. Neurosecretory cells in the

hypothalamus produceantidiuretic hormone (ADH) andoxytocin, which are stored inaxon endings in the posteriorpituitary until they are released.

B. The hypothalamus produceshypothalamic-releasing andhypothalamic-inhibitinghormones, which pass to theanterior pituitary by way of aportal system. The anteriorpituitary produces at least sixtypes of hormones, and some ofthese stimulate other hormonalglands to secrete hormones.

10.3 Thyroid and Parathyroid GlandsThe thyroid gland requires iodine toproduce triiodothyronine (T3) andthyroxine (T4), which increase themetabolic rate. If iodine is available

in limited quantities, a simple goiterdevelops; if the thyroid is overactive,an exophthalmic goiter develops. Thethyroid gland also producescalcitonin, which helps lower theblood calcium level. The parathyroidglands secrete parathyroid hormone,which raises the blood calcium anddecreases the blood phosphate levels.

10.4 Adrenal GlandsThe adrenal glands respond to stress:Immediately, the adrenal medullasecretes epinephrine andnorepinephrine, which bring aboutresponses we associate withemergency situations. On a long-termbasis, the adrenal cortex produces theglucocorticoids (e.g., cortisol) and themineralocorticoids (e.g.,aldosterone). Cortisol stimulateshydrolysis of proteins to amino acidsthat are converted to glucose; in thisway, it raises the blood glucose level.Aldosterone causes the kidneys toreabsorb sodium ions (Na�) and toexcrete potassium ions (K�).Addison’s disease develops when theadrenal cortex is underactive, andCushing’s syndrome develops whenthe adrenal cortex is overactive.

10.5 PancreasThe pancreatic islets secrete insulin,which lowers the blood glucose level,and glucagon, which has theopposite effect. The most commonillness caused by hormonalimbalance is diabetes mellitus, whichis due to the failure of the pancreasto produce insulin and/or the failureof the cells to take it up.

10.6 Other Endocrine GlandsA. The gonads produce the sex

hormones. The thymus secretesthymosins, which stimulate T-lymphocyte production andmaturation. The pineal glandproduces melatonin, which isinvolved in circadian rhythmsand may affect development ofthe reproductive organs.

B. Tissues also produce hormones.Adipose tissue produces leptin,which acts on the hypothalamus,and various tissues producegrowth factors. Prostaglandins areproduced and act locally.

10.7 The Importance of Chemical SignalsIn the human body, some chemicalsignals, such as traditional endocrinehormones and secretions ofneurosecretory cells, act at a distance.Others, such as prostaglandins,growth factors, and neurotransmitters,act locally. Whether humans havepheromones is under study.

10.8 Effects of AgingTwo concerns often seen in theelderly are thyroid malfunctioningand diabetes mellitus.

10.9 HomeostasisHormones particularly help maintainhomeostasis in several ways:Hormones help maintain the level ofnutrients (e.g., amino acids andglucose in blood); help maintainblood volume and pressure byregulating the sodium content of theblood; help maintain the bloodcalcium level; help regulate fuelmetabolism; and help regulate ourresponse to the external environment.

STUDY QUESTIONS1. Explain how peptide hormones and

steroid hormones affect the metabolismof the cell. (p. 207)

2. Contrast hormonal and neural signals,and show that there is an overlap

between the mode of operation of thenervous system and that of theendocrine system. (pp. 209–210)

3. Explain the relationship of thehypothalamus to the posterior pituitary

gland and to the anterior pituitarygland. List the hormones secreted bythe posterior and anterior pituitaryglands. (p. 211)

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230 PART III Integration and Coordination

LEARNING OBJECTIVE QUESTIONSFill in the blanks.

1. Generally, hormone production is self-regulated by a _________ mechanism.

2. The hypothalamus _________ thehormones _________ and _________,released by the posterior pituitary.

3. The _________ secreted by thehypothalamus control the anteriorpituitary.

4. Growth hormone is produced by the_________ pituitary.

5. Simple goiter occurs when the thyroidis producing (too much or too little)_________ because it has (too much ortoo little) _________.

6. Parathyroid hormone increases the levelof _________ in the blood.

7. Adrenocorticotropic hormone (ACTH),produced by the anterior pituitary,stimulates the _________ of the adrenalglands.

8. An overproductive adrenal cortex resultsin the condition called _________.

9. Type I diabetes mellitus is due to amalfunctioning _________ but type IIdiabetes is due to malfunctioning_________.

10. Prostaglandins are not carried in the_________ as are hormones secreted bythe endocrine glands.

11. Whereas _________ hormones are lipidsoluble and bind to receptor proteinswithin the cytoplasm of target cells,_________ hormones bind tomembrane-bound receptors, therebyactivating second messengers.

12. Whereas the adrenal _________ is underthe control of the autonomic nervoussystem, the adrenal _________ secretesits hormones in response to _________from the anterior pituitary gland.

MEDICAL TERMINOLOGY EXERCISEConsult Appendix B for help inpronouncing and analyzing the meaningof the terms that follow.

1. antidiuretic (an”tı-di”yu-ret’ik)2. hypophysectomy (hi-pof”ı-sek’to-me)3. gonadotropic (go”nad-o-trop’ik)

4. hypokalemia (hi”po-kal”e’me-uh)5. lactogenic (lak”to-jen’ik)6. adrenopathy (ad”ren-op’uh-the)7. adenomalacia (ad”e-no-muh-la’she-uh)8. parathyroidectomy

(par”uh-thi”roy-dek’to-me)

9. polydipsia (pol”e-dip’se-uh)10. dyspituitarism (dis-pı-tu’ı-ter’izm)11. thyroiditis (thi-roy-di’tis)12. glucosuria (glu-co-su’re-uh)13. microsomia (mi’kro-so’me-uh)

4. Give an example of the negativefeedback relationship among thehypothalamus, the anterior pituitary,and other endocrine glands. (pp. 211–213)

5. Discuss the effect of growth hormoneon the body and the result of having toomuch or too little growth hormonewhen a young person is growing. Whatis the result if the anterior pituitaryproduces growth hormone in an adult?(p. 213)

6. What types of goiters are associatedwith a malfunctioning thyroid? Explaineach type. (pp. 214–215)

7. How do the thyroid and theparathyroid work together to controlthe blood calcium level? (pp. 215–216)

8. How do the adrenal glands respond tostress? What hormones are secreted bythe adrenal medulla, and what effectsdo these hormones have? (pp. 216–218)

9. Name the most significantglucocorticoid and mineralocorticoid,and discuss their functions. Explain thesymptoms of Addison’s disease andCushing’s syndrome. (pp. 216–218)

10. Draw a diagram to explain how insulinand glucagon maintain the bloodglucose level. Use your diagram to

explain the major symptoms of type Idiabetes mellitus. (pp. 220–221)

11. Name the other endocrine glandsdiscussed in this chapter, and discussthe functions of the hormones theysecrete. (pp. 223–224)

12. What are leptin, growth factors, andprostaglandins? How do thesesubstances act? (pp. 224–225)

13. Discuss five ways the endocrine system helps maintain homeotasis. (pp. 227–228)

WEBSITE LINKVisit this text’s website at http://www.mhhe.com/longenbaker7 for additional quizzes, interactive learning exercises, and other study tools.

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