INTEGRATED ACTION OF HORMONES ON FUEL METABOLISM

INTRODUCTION
Feeding
Metabolic fuels (glucose, amino acids, fatty acids) Insulin

Fasting & Energy demand

Stored energy forms (triglyceride, glycogen, protein) Glucagon, Epinephrine, Norepinephrine Cor tisol GH Energy utilization Prevention of Hypoglycemia

Storage (Energy reser ves) & Building Enhanc es formation of complex storage form Inhibits utilization of fuel molecules

ADIPOSE TISSUE
Re-esterification rate Basal -20 % Energy demand 10 % Variation in lipolysis varies by 10 fold Insulin cAMP catecholamine (T3, Cortisol, GH) GH Lipolysis after 2 hr GH and cortisol reduces insulin responsiveness and reduces reesterification

MUSCLE
Insulin Glucose
Minutes

Glucose
Pyruvate Lactate Glycogen

hours

Serum FFA

GH Cortisol

Protein

cAMP Epinephrine Norepinephrine

Amino acids

LIVER
Insulin promotes storage of glucose as glycogen Reduces the release of glucose Inhibits glycogenolysis, gluconeogenesis, and ketogenesis Stimulates the synthesis of fatty acids and proteins. Glucogon antagonizes insulin action on liver Epinephrin & norepinephrin acts by augmenting cAMP level and acts similar to glucogon Cortisol acts as permissive agent for the action of glucogon and catecholamines Cortisol ensures supply of aminoacids for gluconeogenesis by it action on muscle protein T3 increases glucose utilization by increasing glucose metabolizing enzyme GH helps liver gluconeogenesis by mobilizing FFA from other tissues. Contributes to ketogenesis
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PANCREAS
Glucogon stimulates insulin Insulin inhibits glucogon Alpha cells require insulin to sense glucose Insulin is required for normal secretor y response of -cell for Glucose Epinephrin and nor epinephrin stimulate glucogon secretion and inhibits insulin GH, cor tisol and T3 maintains normal secretor y response GH, cor tisol exaggerates the response of -cell to hyperglycemia When GH, cor tisol are present more insulin is required Excess of GH and cor tisol in blood results in diabetes Diabetogenic ef fect of chronic glucocor ticoid therapy
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FEEDING AND FASTING

Postprandial period Postabsorptive period Fasting period

POSTPRANDIAL PERIOD
Feeding sequestration and storage Cephalic (Ach & VIP) innervates endocrine of pancreas

Food GIP GLP

Glucose, Amino acids in blood

-cell

Insulin (10

50 U/ml)

AA GH

Glucose FA AA

Glycogen Triglyceride Protein

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Glucogon

POSTPRANDIAL PERIOD
Extrahepatic tissues use glucose from dietary source than from Glucose form liver and FA from adipose Total carbohydrate ( 1/2) => Hepatic glycogen FA mobilization inhibited by insulin

POSTABSORPTIVE PERIOD
Energy is drawn from storage depots Insulin conc. lowers and controlled by glucose conc. 90 mg/ml From liver, glucose released - 75% from Glycogen & 25% from gluconeogenesis induced by glucogon Glucogon level is low but low insulin level results in effective action of glucogon Cortisol and GH secreted at basal rate 75 % glucose taken by brain, blood and other tissues (Insulin independent) 25 % glucose taken by Muscle and adipose tissue (Insulin dependent)
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POSTABSORPTIVE PERIOD
FFA release increases due to low insulin level Glucose metabolism in muscles decreases Liver glycogen gets gradually depleted and glucose is synthesized by neogenic pathway using AA and glycerol

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FASTING
More than 24 hours after the last meal, the individual can be considered to be fasting Circulating insulin decrease. Glucogon and GH increase Glucocorticoids and GH reduces glucose utilization in muscle and adipose tissue Reduction in insulin level causes lipolysis to increase FA re-esterification decreases, more FA are mobilized FA mobilization enhanced by GH and cortisol Reduced insulin leads to breakdown of muscle protein, AA supplied for gluconeogenesis
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METABOLISM DURING FASTING

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GH ON BLOOD GLUCOSE

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HORMONES DURING FASTING

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REFERENCE
Goodman, H. Maurice. Basic medical endocrinology. Academic Press, 2010.

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Thank You
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