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INTEGRATED ACTION OF

HORMONES ON FUELMETABOLISM

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Metabolic fuels (glucose, amino

acids, fatty acids)

Insul in

Storage (Energy reserves) & Bui lding

Enhances formation of complex

storage form

Inhibits uti l ization of fuel molecules

INTRODUCTION

Stored energy forms (tr iglyceri

glycogen, protein)

Energy uti l ization

Prevention of Hypoglycemia

Glucagon,

Epinephrine,

Norepinephri

Cortisol

GH

Feeding Fasting & Energy demand

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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 re-

esterification

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Pyruvate

Lactate

MUSCLE

Serum

FFA

Insulin

Glucose

Glycogen

GlucoseMinutes

hours

Epinephrine

Norepinephrine

cAMPGH

Cortisol

Amino acids

Protein

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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.

Glucogonantagonizes insulin action on liver

Epinephrin & norepinephrin acts by augmenting cAMP level and acts similar tglucogon

Cortisol acts as permissive agent for the action of glucogon and catecholamin

Cortisol ensures supply of aminoacids for gluconeogenesis by it action on mu

protein

T3 increases glucose utilization by increasing glucose metabolizing enzyme

GH helps liver gluconeogenesis by mobilizing FFA from other tissues. Contribuketogenesis

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Glucogonstimulates insulin

Insulin inhibits glucogon

Alpha cells require insulin to sense glucose

Insul in is required for normal secretory response of -cell for

Glucose

Epinephrin and nor epinephrin stimulate glucogon secretion andinhibits insulin

GH, cortisol and T3 maintains normal secretory response

GH, cortisol exaggerates the response of -cell to hyperglycemia

When GH, cortisol are present more insulin is required

Excess of GH and cortisol in blood results in diabetes Diabetogenic effect of chronic glucocorticoid therapy

PANCREAS

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Postprandial period

Postabsorptive period

Fasting period

FEEDING AND FASTING

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Feeding sequestration and storage

Cephalic (Ach & VIP) innervates

endocrine of pancreas

Food GIP GLP -cell Insulin (10 50U/

Glucose, Amino acids in blood

AAGH Glucogon

POSTPRANDIAL PERIOD

Glucose Glycogen

FA Triglycer

AA Protein

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Extrahepatic tissues use glucose from dietary source thanfrom Glucose form liver and FA from adipose

Total carbohydrate (1/2) => Hepatic glycogen

FA mobilization inhibited by insulin

POSTPRANDIAL PERIOD

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Energy is drawn from storage depots Insulinconc. lowersand controlled by glucose conc. 90 mg/

Fromliver, glucose released - 75%fromGlycogen & 25%fro

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)

POSTABSORPTIVE PERIOD

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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

POSTABSORPTIVE PERIOD

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More than 24 hours after the last meal, the individual canconsidered to be fasting

Circulating insulin decrease. Glucogon and GH increase

Glucocorticoids and GH reduces glucose utilization in mus

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

FASTING

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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