04 21-22 Glycogen Lavers

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Carbohydrate Storage and

Synthesis in Liver and Muscle:Glycogen

Copyright 1999-2004 by Gene C. Lavers

No part of this presentation may be reproduced by any mechanical, photographic, or electronic process, or inthe form of a phonographic recording, nor may it be stored in a retrieval system, transmitted, or otherwise

copied for public or private use, without written permission from the publisher.

Lecture 21 and 22

Baynes & Dominiczak, Chapter 12Gene C. Lavers, Ph.D. [email protected]/~glc1


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Copyright 1999-2004 by GeneC. Lavers

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Glycogen 12 topics Carbohydrate Metabolism Investing for the future Outline of Topics

IntroductionStructure of Glycogen highly branced a 1,4)-glucose polymerGlycogenesis Glc incorporated into glycogen (liver & muscle, kidney)Glycogenolysis Glucose mobilized from glycogen in liver and muscle

Hormonal regulation of hepatic glycogenesis vs. glycogenolysis insulin vs. glucagonMechanisms of glucagon action Signals phosphorylations, pathways flip Glycogenolysis in liver plasma glycemia maintenance: acute vs. postabsorbtive Glycogenolysis in muscle Mobilizing glucose for ATP contraction activityRegulation of glycogenesis replenish glycogen stores vs. immediate needsGluconeogenesis de novo ( new) glucose from non carbohydrate carbon skeletonsRegulation of gluconeogenesis De novo glucose synthesis fueled by fat oxidation Interconversions of fructose/galactose/mannose/glucose glycoproteins, etc., Inborn errors of metabolism glycogen storage diseases

Glucose Fuel Storage and mobilization for oxidaton


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Metabolic Fate of Glucose Glycogen Metabolism Introduction

Red cells and the brain Have an absolute requirement for bloodglucose for their energy metabolism.

These cells consume about 80% of the glucose (200 g , 1.1 mol, ca.1500 kcal ) consumed per day by a 70 kg human , in good health.

Blood and extracellular fluid volume contains about 10 g glucose must be replenished constantly .

Assumes a blood volume = 7 L, hematocrit = 45%, and no other

distribution system operates.Normally, blood [glucose] range is between 4 6.5 mM = glycemia

(about 80 120 mg/dL)


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Hypoglycemia hyperglycemia - glycemia Glycogen Metabolism[glucose], in blood plasma Introduction

hypoglycemia ( 4 2.5 mM, 45 mg/dL);

extreme hypoglycemia, 6.5 mM) lasts 2- 3 hrs, glycemia

homeostasis glycemia maintained: ~ 4-5 mM (80-100

mg %), resting [glucose]. Such control due to: in part, glycogen synthesis (alltissues). Up to max of 1 2 % of muscle tissue wt(work) and 4 6 % liver wt for later release ofglucose from liver to supply glucose to body.

Before meal

After meal

Post meal

Prandial (meal): preprandial, postprandial, postabsorptive


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Glycogenesis vs. glycogenolysis Glycogen MetabolismLiver maintains blood [glucose] Cyclic responses

Fig. 12.1 Sources of Blood Glucose.

Glucose stored as glycogen:highly branched dendrite-likepolymer, a polysaccharide.Glycogenesis glycogensynthesized during and aftera meal.

Glycogenolysis releasesglucose into blood (Like acontrolled time-release)

Total heptic glycogen stores barely able to maintain blood[glucose] beyond 12 hour(fasting).

Gluconeogenesis makes new glucose during post absorptive state,before meals, and during sleep. Glycogenolysis declines to neardepletion of glycogen after 12-24 hrs Liver uses gluconeogenesis tomaintain blood [glucose].


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6

Glycogen Storage Carbohydrate Metabolism Various Tissues Structure

Blood glucose = 10 g, tissues needs easilydeplete.Glycogen degraded to glucose-1P G6P

for oxidative metabolism in tissues tosynthesize ATP.Liver: G6P G + P, by G6P phosphatase .Muscle lacks G6P phosphatase .

Fig. 12.2 Tissue distribution ofcarbohydrate energy reserves(70 kg adult).

Fig. 12.3 Close-up ofglycogen structure.

Highly branched dendritic polymer


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Structure of Glycogen Carbohydrate Metabolism Properties

KEY FEATURES

non reducingend

a -1,6 acetallinkage

a -1,4 acetallinkage

a

O

O

Oa 16

14

C O

OH

H

C O

O C

H

reducing end hemiacetal

acetal

enedicts

solut on

C C

OH

H

alcohol


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8

Glycogen metabolism Carbohydrate Metabolism Anabolism vs. Catabolism Comparison

Glycogenesis

Glucose glycogen 5 steps

1. Glucokinase2. Phosphogluco-

mutase3. UDP-Glc PPase4. Glycogen

synthase

5. Branching GlycogenolysisGlycogen glucose

4 steps1. Glycogen

phosphorylase

2. transglycosylase3. transglycosylase4. G6Pase

____________Regulatory enzymeRate-limiting enzyme

Fig. 12.4 Glycogenesis (L)Glycogenolysis (R)

Different enzymes


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Glycogenesis Carbohydrate Metabolismvs. glycolysis, PMP In: Liver, Muscle, Adipose tissues

Portal blood: delivers glucose-rich blood to liver during/shortly after a meal . Liver rich in GLUT-2: high capacity, low affinity (k m >10 mM), high glucose flux .

Glucokinase (GK): gene induced by continuous glc-rich diet.GK K m ~ 5-7 mM: activity when portal blood [Glc] above 5 mM.GK not G6P inhibited : thus G6P pushed into all pathways glycolysis, PMP, and

glycogenesis (muscle uses lipid oxidative metabolism for ATP).Fate of excess glucoseIn Liver: goes to

glycogenesis reserve : for maintaining post absorptive blood [glc].glycolysis: after glycogen reserve is full.

energy/ATP synthesis and triglycerides: FAS and TGs exported toadipose tissue for storage.In muscle: glucose stored in glycogen; glycolytic pyruvate formed.In adipose: glucose DHAP glycerol TGsIn RBC: glucose pyruvate lactate; NADPH (protect from ROS)

Priority: favor synthesis of glycogen first: save first!


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Copyright 1999-2004 by GeneC. Lavers 10

Fate of diet fuels Carbohydrate Metabolism Glucose is central metabolite Overview of Topics

DIETDigestion and Absorption

Glucose

carbohydrate fatprotein

amino acids TGs

liver

Transport via portal vein

intestines

amino acids

GLYCOGEN musclesmovement

gluconeogenesis

brain

glycogenolysis

GLUCOSE

GLUCOSE

GLYCOGEN

organs

glycogenesis glycogenolysis

glycogenesis

Transport via blood vessels


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Hormonal control Carbohydrate MetabolismGlycogenolysis In Liver Comparison

Glycogenolysis: response to lowblood [glc] from:Post absorptive utilization.Response to stress.

3 hormones activation mode:Glucagon 3.5 kd peptide, from a -cells of endocrine pancreas; mainfunction: activate hepaticglycogenolysis to maintainnormoglycemia.

Epinephrine tyrosine derivative, acatecholamine from adrenal

medulla activates glycogenolysis inresponse to acute stress .

Cortisol adrenocortical steroidvaries diurnally in plasma, but maybe chronically elevated undercontinuously stressful conditions.

Glucagon, Epinephrine, Cortisol, Insulin

Fig. 12.5 Hormones involved in control ofglycogenolysis.


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Glucagon Carbohydrate MetabolismIn Liver Hormonal Regulation of Glycogenolysis

Glucagon 3500 MW protein (29-aa): secreted by a -cellsof endocrine pancreas, activates glycogenolysis tomaintain normal glycemia, when blood [glucose] becomes

hypoglycemic.Glucagon t/2 ~ 5 minutes. (removal from blood by receptorbinding, renal filtration, proteolytic inactivation in liver.)

Elevated blood [glucagon]: between meals; chronically

elevated during fasting or low-carbohydrate diet.Decreased blood [glucagon]: decreases during and soonafter a meal ([glucose] is very high).

Glucagon, epinephrine (adrenalin), cortisol, insulin


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Acute & Chronic Stress Carbohydrate MetabolismGlycogenolysis Activation

Physiologic -- in response to increased blood glucoseutilization during prolonged exercise.

Pathologic -- as a result of blood loss .

Psychological -- in response to acute or chronic threats .

Acute stress (regardless of source): activates glycogenolysisthrough the action of catecholamine hormone, epinephrine

(released by the adrenal medula) .During prolonged exercise: both glucagon and epinephrinecontribute to stimulation of glycogenolysis.

Glycogenolysis is activated in response to stress

l


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Insulin Carbohydrate MetabolismHormonal regulation Inhibition of Glycogenolysis

Insulin secreted by pancreas b-cells when blood [glucose] is high.

Synthesized as single peptide chain zymogen: proinsulin.

In secretory granules, selective proteolysis releases an internalpeptide and a 2-chained (via 2 -S S- ) insulin hormone.

Insulin elicits uptake and intracellular use or storage of glucose,an anabolic hormone.

Hyperglycemia results in elevated blood [insulin] associated withfed state.

Hyperinsulinism associated with insulin resistance and ifchronic can lead to diabetes type-2 and related pathologies.

Antagonist of glucagon, epinephrine (adrenalin) , cortisol


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Glycogen Carbohydrate Metabolism Signal Transduction Regulation Mechanism

Fig 12.6 Mobilization of liverglycogen by glucagon.

1. Glucagon binds hepatic membrane receptor :activates cascade reactions .

2. G-protein-GDP in resting state: releasesGDP, a -subunit binds GTP.

3. G-protein-GTP: conformation change, releases a -subunit:GTP complex.

4. a -GTP binds to adenylate cyclase (AC) .5. AC converts ATP cAMP (+PP; 2 P).

6. cAMP binds regulatory subunit of proteinkinase A : active catalytic subunit released= PKA.

7. PKA phosphorylates 3-enzymes: uses ATP Inhibitor 1 inhibitor-1 (+P) ACT.

phosphorylase kinase b PKa (+P) ACT. glycogen synthase a b (+P) INACT.


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Glycogen Carbohydrate Metabolism Signal Transduction Regulation Mechanism

Fig 12.6 Mobilization of liverglycogen by glucagon.

PKA phosphorylates 3-enzymes: uses ATP Inhibitor 1 inhibitor-1 (+ P) ACT. Phosphorylase Kinase b PK a (+ P) ACT. Glycogen Synthase a GS b (+ P) INACT.

Phosphorylase kinase a : uses ATPGlycogen Phosphorylase b GP a (+P)

7. Glycogen Phosphorylase a : glycogenolysisreleases G1P

8. Inhibitor 1-P keeps phospho-protein

phosphatase ( PPP ) inactive: glycogendegradation continues.


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Glycogen Carbohydrate Metabolism Reciprocal Synthesis and Degradation Regulation Mechanism

Glu 1P

Phospho rylase a

Glycogen synthase I

Glycogen synthase D

Phosphorylase b b

PhK

ATP

ADPa

PPP

p

IPhK

ADP

ATP

D PPP

p

inactive

active

inactive

active

glycogen

Phosphorylation-Dephosphorylation PPP = Protein Phosphatase


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Balancing Pathway Activities Carbohydrate MetabolismAvoiding futile cycles Inhibiting glucose

Prandial glucose used up, glycemia falls into hypoglycemia.

Glucagons enzyme cascade amplification turns on liverglycogenolysis balanced inhibition of glycogenesis. Also producesinhibition of

Protein synthesis uses considerable ATP and GTPCholesterol synthesis uses ATP Fatty acid (FA) synthesis uses ATP to activate acetyl CoA (malonyl CoA)Triglyceride (TGs) synthesis from glycolytic DHAP derived from glucoseGlucose synthesis (gluconeogenesis) uses GTP

Glucose utilization (glycolysis) uses ATPKey enzymes phosphorylated in opposing pathways, avoids futile cycles.

Glucagon shifts liver metabolism to keep blood [glc] glycemic tomaintain vital body functions (see Ch 20) .

Glycogenolysis floods system with G1P, G6P, and glucose


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Termination of glucagon response Carbohydrate MetabolismMust be rapid Hepatic mechanisms

Rapid, redundant shutdownmechanisms: accompany blood[glucagon] . Enzyme cascade foramplifying glycogenolysis activation isvia dephosphorylaton.

1. Ga -GTP Ga -G DP: by phosphodiesterase2. Phosphodiesterase : cAMP AMP

3. [cAMP] , R-cAMP dissociates4. 2R + 2C R 2C2 : adenylate cyclaseinactive again .

5. PhosphoProtein Phosphatase (PPP):removes- P ;

all enz-P enz + P;glycogenolysis stops. Inhibitor 1, increases PPP activity .

Glycogenolysis stops. Decreased blood [glucagon] accompaniesrise in blood [glucose] .

Fig. 12.7 Mechanisms of terminationof hormonal response to glucagon.


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Glycogen-storage Diseases Carbohydrate MetabolismInherited Metabolic Diseases Inborn errors of Metabolism

Six rare genetic diseases affect glycogen synthesis at differentenzyme deficiency steps in the pathway.

Fig. 12.8 Major classes of glycogen-storage diseases.

E i h i C b h d M b li


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Epinephrine Carbohydrate Metabolism Hormonal Regulation Activation of Glycogenolysis

Epinephrine ( Adrenaline ) and precursor (norepinephrine alsohormonally active), derived from tyrosine. Adrenal gland cells releasewhen neural signals trigger the fight-or-flight response; many diversephysiological effects follow.

Epinephrine stimulates release of G1P from glycogen; produceselevated intracellular [G6P]. Glycolysis increases in muscle; liverreleases glucose into the bloodstream.

Glucagon, Epinephrine, Cortisol, Insulin

HONH 3 +

COO-

HO NH 2 +

CH3

HO

HOtyrosine

L-dopa

HO NH 3 +

HO

HO

epinephrinenorepinephrine

E i h i


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Epinephrine Carbohydrate MetabolismMobilizing hepatic glycogen Second Messengers

Epinephrine binds to a - and b-adrenergic receptors.Two pathways stimulated.b-receptor: similar to glucagonmechanism. G-proteins, cAMP .

Epinephrine response: augmentsglucagons during severehypoglycemia : rapid heartbeat,sweating, tremors and anxiety.

a -receptor: G-proteins , active membraneisozyme of phospholipase C (PLC):specific for cleavage of membranephospholipid (PL), and PIP 2. PIP 2 DAG +IP 3 , 2nd messengers.DAG activates PKC (like PKA).

IP 3 promotes Ca 2+ into cytosol.Ca 2+ binds calmodulin: activates

phosphorylase kinase , leads to activationof glycogen phosphorylase : glucosereleased to blood.

Fig. 12.9 Glycogenolysis viaa -adrenergic receptor

P i ki A i M l


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Protein kinase A in Muscle Carbohydrate MetabolismDuring Exercise Activating Glycogenolysis

Muscle reacts to epinephrinenot glucagon.b-adrenergic receptor (cAMP)activates glycogenolysis for:

Fight or flightProlonged exercise

2 hormone independent modes:Influx of Ca 2+ activates

phosphorylase kinase via Ca 2+ calmodulin complex.

AMP activates phosphorylasedirectly2 ADP ATP + AMP; [AMP]

AMP activates phosphorylase .

Muscle lacks glucagon receptorand G6Phosphatase enzyme.

Fig 12.10 Regulation of PKA

in muscle.

l ff b l


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Regulatory effects by Insulin Carbohydrate MetabolismReceptor dimerization Glycogenesis

Insulins 2 main functions: lowers blood glucose byreversing the effect ofglucagons phosphorylationof enzymes and proteins.

Stimulates gene expression

of carbohydrate metabolismenzymes.

Fig 12.1 1 Regulatory effects of insulin onhepatic and muscle carbo metab.

Gl i (GNG) C b h d M b li


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Gluconeogenesis (GNG) Carbohydrate MetabolismGlucose from non carbohydrates Cytosol-Mitochondrion

Gluconeogenesis: essential during fasting andstarvation, when hepatic glycogen depleted, tomaintain blood glucose . Energy and carbon source required:oxidation of FA released from adipose tissueprovides ATP; carbons from 3-sources.Lactate from RBC and active muscle.

Large muscle mass: major source ofglucogenic amino acids; transamination.Glycerol from TGs: DHAP via glycerol-3P.3 glycolytic irreversible reactions: PK, PFK-1, GK bypassed by phosphatases: FBPase, andG6Pase after PEPCKase1,3BPG 3PG is reversible, DG similar.Lactate cycle: Cori cycle (ch 20). Muscle lactate and pyr liver-GNG glc, to muscle-glycolysis lactateGlucose-alanine cycle: [muscle: glc pyr

ala ] [liver: GNG glc] [muscle: glc pyr ala ]

3-Sources: Lactate, amino acids, glycerol

Fig 12.12 Pathways of gluconeogenesis.

R g l ti g gl g i C b h d M b li


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Regulating gluconeogenesis Carbohydrate MetabolismHormonal mechanisms Glycolysis vs. Gluconeogenesis

Gluconeogenesis vs. glycolysis: avoid a futilecycle; active GNG inhibit glycolysis Enz- P or inactive GNG active glycolysis. EnzF26BP: allosteric (+) regulator of F16BP . Made by:PFK2 : F6P F26BP ; enhances glycolysis.F26BPase : F6P F26BP ; enhances GNG .

PFK2 / F26BPase : a bifunctional, with P switch: PFK2 /F26BPase PFK2 /F26BPase -PPFK1 : F6P F16BP; F26BP Rx rate ! F16BPase : F6P F16BP; F26BP inhibits GNG ![acetyl CoA ]: slows TCA; act. PC [OAA ] Glc

Glucagon: promotes phosphorylation (PK , inact.) Insulin: promotes de -phosphorylation ( PK act.)

During fasting: glucagon , PK -P inact , GNG , EM Eat Carbo meal: insulin , PK act, GNG , EM

Control: liver PFK1 and F1,6BPase

Fig. 12.13 Gluconeogenesisregulated by heptic[F26BP] and[acetyl CoA]

F t d g l t C b h d t M t b li


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Fructose and galactose Carbohydrate MetabolismSugar Interconversions Other sugars

a -D-Glucose

Triose-P

OO O

a -D-Galactose-D-Fructose

Exclusively in liver

pyruvate

glycolysis

(P ) (P)(P) (P )

(P )a a a

b

pyruvate

glycolysisgluconeogenesis

OAA

PC

Acetyl CoA

PDH

epimers

+

PEP

PEPCK

aldose aldoseketose

l f


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Hormonal features Carbohydrate MetabolismRegulation Gluconeogenesis

Fig. 12.14 Features of hormone action. Multihormonalregulation of gluconeogenesis illustrates fundamentalprinciples of hormone action


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Carbohydrate Storage and Synthesisin Liver and Muscle

END

M t b li F t f Gl Gl M t b li


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Metabolic Fate of Glucose Glycogen Metabolism Introduction

Red cells and the brain Have an absolute requirement forblood glucose for their energy metabolism .

These cells consume about 80% of the glucose (200 g, 1.1 mol,ca. 1500 kcal) consumed per day by a 70 kg human, in good health.

Blood and extra cellular fluid volume contains about 10 gglucose, which must be replenished constantly.

Assumes a blood volume = 7 L, hematocrit = 45%, and noother distribution system operates.

Normally, blood [glucose] range is between 4 6.5 mM(about 80 120 mg/dL)

Gl i Gl M b li


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Gluconeogenesis Glycogen Metabolism

A backup system makes new glucose Introduction

Liver can synthesize glucose from non carbohydrate precursors.

Amino acids supply carbon skeletons, as does glycerol.

During starvation*, liver uses degraded muscle protein asthe primary precursor of glucose; also lactate (fromglycolysis) and glycerol (from fat) .

Fatty acids from triacylglycerides (TAGs) mobilzed (fromadipose tissue**) provide the energy for gluconeogenesis.

__________________________* Metabolically may begin about 12 hours after the last meal.** During well-fed states, excess glucose is converted to triacylglycerides

(TGs) in adipose cells.

GLUT 2 T t C b h d t M t b li


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GLUT-2 Transporter Carbohydrate Metabolism In liver Crossing the plasma membrane

A high capacity GLUT-2 transporter (low-affinity, km>10 mM) allows glucose free entry into and exit fromliver cells across the plasma membrane.

Liver cells have a large number of GLUT-2, so high[glucose] coming from the portal blood can easily enterthe cytoplasm.

GLUT-2 transporter getting GLUCOSE in and out of cell

Gl ki C b h d M b li


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Glucokinase Carbohydrate Metabolism In liver Preparing G-6-P

Glucokinase (GK) specifically phosphorylates glucose toglucose-6-phosphate (G6P) trapping glucose inside cell.Liver has copious amounts of GK.

GK gene is inducible (more GK made) when a highcarbohydrate diet is continued .

Km GK ~ 5 7 mM, GK becomes more active when portal

blood [glucose] exceeds 5 mM (100 mg %).G6P is not a product inhibitor of GK! (G6P inhibits hexokinase)

Keeping glucose in the cell investing for metabolism

P th ti f G6P C b h d t M t b li


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Pathway options for G6P Carbohydrate Metabolism In liver Pathways in the cytosol

After a carbohydrate meal, G6P floods the cell via GKG6P forced into several major pathways:

Glycogenesis yields highly branched, dense glucose

polymer. After glycogen is replenished, then

Glycolysis oxidizes excess G6P to pyruvate (andlactate) for energy production and triglyceride (TAG)synthesis for export to adipose cellsand

Pentose phosphate pathway yields NADPH (andribose and other sugars) for fatty acid synthesis (theregoes the waistline!)

What fates await G6P?

Activated UDP -Glucose Carbohydrate Metabolism


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Activated UDP Glucose Carbohydrate MetabolismPolymerization step Glycogenesis pathway

UDP-Glucose adds glucose to glycogen via Glycogen Synthase

Glucose 6PGlucose 1PUDP-GlucoseGlycogenn+1

UDP-glucose pyrophosphorylase

123

12

3 Glycogen Synthase

Phosphoglucomutase

Three-step Pathway

UTPpp

HOO

O pOHHOOH

H

pU pp pU

pp

2

2

Glucose 1P

Regulatedstep

activated

p + p

Gl i C b h d t M t b li


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Glycogenin Carbohydrate MetabolismGlycogenesis

{Octamer of Glucose glycogenin protein} primer

Glycogen Synthase requires glycogen primereight a -1,4-linked glucose residues (at least) .

Primer = Glucose 8 Tyr C1 Glycogenin (Mr 37,000 protein) .

Glycosyltransferase adds C 1 of Glu 1 -ppU to a tyrosyl residue ofGlycogenin ; 7 UDP-Glu yield 8-mer Glucose 8 -Glycogenin protein primer .

Glycogen Synthase adds glu of UDP-glu to non reducing C 4 -OH ofGlucose- Glycogenin synthesizing a glycogen 50,000 polymer. amylo-(1,4 to 1,6)-transglycolase creates the branches; transfers6-mer to the C

6-OH so 4-residues separate branches formed by a -1,6-

acetal linkage.

All the enzymes required are associated with the glycogen for rapidsynthesis of glycogen

Branching Glycogen Carbohydrate Metabolism


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Branching Glycogen Carbohydrate Metabolisma -1,6 acetal linkage Glycogenesis pathway

UDP-glucose

GlycogeninHO

1. Glucosyl-

transferase

2. Amylo-1,4 1,6-transglycosylase

3. Glycogen Synthase

O

1

7 + 1

O

6

4

O

O6

O

3

Glycogen synthase Carbohydrate Metabolism


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Glycogen synthase Carbohydrate MetabolismA principle? Regulation

Step 3, Glycogen synthase is regulated, not 1 or 2

Regulate a pathway after a branch branch*

UDP-glucose

Glycoproteins

Glycolipids

Other sugarsGlycogen

Glucose-1P

Regulate here?

Regulate here.

___________________________________________* Recall: Does the regulated, committed step of glycolysis (F1,6BP) follow this principle?

Polysaccharide Phosphorylases Carbohydrate Metabolism


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Polysaccharide Phosphorylases Carbohydrate Metabolism

In Liver Glycogenolysis

Using phosphate to cleave C O bonds: phosphorolysis

* Glucose stored asglycogen or starch animals plants

Glycogen

Muscle

Liver

P OO

O

O

HOO

OP OHHO

OHH HO O

OR-1OH

HO

OHH

+

Glucose 1P Glycogen n-1

P+

4-residues

from branch

~ribosome

Non-reducing end

P

P

Branch point

Glycogen Phosphorylase Carbohydrate Metabolism


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BrainRBC

Fat cellsPeripheral tissues

Glycogen Phosphorylase Carbohydrate MetabolismLiver vs. Muscle Glycogenolysis Pathway

Glycogen Glucose 1P

[ATP]

Muscle

Liver

Glucose 6P Glycolysis

TCAGlucose 1P

Glucose 6P

Glucose

Glucose

Fate of glycogen glucose

+

CO2 + H 2 O

[AMP]

3 ATP

GlucoseHex Kinase

2 ATP

P Glc mutase

G6Pase

ATP

ADP

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04 21-22 Glycogen Lavers