INSULIN GLUCAGON EPI- NEPHRINE CORTISOL Role in metabolic Homeo- stasis Major anabolic hormone; Promotes storage of nutrients, glucose uptake in liver, adipocytes, skeletal muscle; Regulates glucagons; synthesized & released in response to change in blood fuel levels Counterregula tes insulin; Maintains fuel availability in absence of dietary glucose; Acts on liver and adipocytes; Synthesized & released in response to change in blood fuel levels Insulin counterreg ulatory hormone Insulin counterregu latory hormone Signal Trans- duction Mech. Binds to pl mem receptor on target cell Receptor cytosolic side has tyrosine kinase activity Receptor coupled to AC and cAMP production Catecholam ine: act as either NTS, or Hormone Binds intracellul ar receptors acts on nuclear chromatin Bl. Glu. Levels required for release High Low Low Low Type of receptor Tyrosine Kinase AC coupled receptor x x Intra- cellular 2 nd Msgr Insulin receptor substrate (IRS-1) cAMP x x MOA o Reverses glucagons-stimulated phosphorylation o Uses phosphorylation cascade to phosphorylate several enzymes o Induces & represses synthesis of certain enzymes o Acts as growth factor to stimulate protein synthesis o Stimulates glucose & aa uptake into cells o Activated ProtKinaseA phosphorylates Ser residues of reg. enz. in fat & carb metab. Acts on CREBs to initiate enz transcription Signal Receptor internalization, o Termination of G s protein activation

Insulin vs. Glucagon vs. Epinephrine vs. Cortisol

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INSULIN GLUCAGON EPI-NEPHRINE

CORTISOL

Role in metabolic Homeo-stasis

Major anabolic hormone; Promotes storage of nutrients, glucose uptake in liver, adipocytes, skeletal muscle;Regulates glucagons; synthesized & released in response to change in blood fuel levels

Counterregulates insulin; Maintains fuel availability in absence of dietary glucose; Acts on liver and adipocytes; Synthesized & released in response to change in blood fuel levels

Insulin counterregulatory hormone

Signal Trans-duction Mech.

Binds to pl mem receptor on target cellReceptor cytosolic side has tyrosine kinase activity

Receptor coupled to AC and cAMP production

Catecholamine: act as either NTS, or Hormone

Binds intracellular receptors acts on nuclear chromatin

Bl. Glu. Levels required for release

High Low Low Low

Type of receptor

Tyrosine Kinase AC coupled receptor x x

Intra-cellular 2nd Msgr

Insulin receptor substrate (IRS-1) cAMP x x

MOA o Reverses glucagons-stimulated phosphorylationo Uses phosphorylation cascade to phosphorylate

several enzymeso Induces & represses synthesis of certain enzymeso Acts as growth factor to stimulate protein

synthesiso Stimulates glucose & aa uptake into cells

o Activated ProtKinaseA phosphorylates Ser residues of reg. enz. in fat & carb metab.

Acts on CREBs to initiate enz transcription

Signal Termi-nation

Receptor internalization,Low glucose levels cause rapid removal from circulation and degradation in liver

o Termination of Gs protein activation (GTP hydrolysis)o Phosphodiesterase degradation of cAMPRapid signal termination

Gen’l Effects Anabolic, uptake glucose, store nutrients Mobilization and utilization of nutrients

Structure Polypeptide, two strands held together by 2 disulfide bondsCoprecipitates w/ Zinc ions, due to insolubility

Polypeptide, 29 aa, MW 3,500Plasma T1/2 is 3-5min.

Site/Mode of Synthesis

cell of pancreasPreprohormone on ribosome of rERProhormone in rER, forms disulfide bondsPackaged in GolgiC-peptide cleaved out in storage vesicles containing zinc ions

cell of pancreasPreprohormone on ribosome of rERProhormone in rER lumenProteolytic cleavage to 29aa mature glucagon

Site/Mode of Secretion

High glucose levels through GLUT-2high ATP levelsinhibits K+pump to allow ions out of celldepolarization of membrane due to Ca2+

influxfusion of exocytotic vesicles w/pl mem to release insulin to blood stream (passes peripheral cells to suppress glucagon secretion

Regulated by [glucose] & [insulin]Secretes into pancreatic ducts bloodsteam