The following points highlight the seven major endocrine influences on metabolism of carbohydrates. The endocrine influences are: 1. Insulin 2. Adrenocortical Hormones 3. Anterior Pituitary Factors 4. Epinephrine 5. Thyroid Hormone 6. Glucagon 10. Sex Hormones.

1. Insulin:

a. Causes glucose transport across cell mem­brane by increasing the permeability of the cells.

b. Increases glycogen formation in liver and muscle by stimulating hexokinase and glycogen synthetase.

c. Accelerates the conversion of glucose to fat.

d. Stimulates protein synthesis.

e. Inhibits ketogenesis.

f. Inhibits gluconeogenesis.

g. Increases glycolysis by stimulating hex­okinase and phosphofructokinase in liver and muscle.

h. Has effect on muscle ion balance.

i. Causes initial phosphorylation (hexokinase reaction) of glucose for further oxi­dation.

The sulfonylureas e.g., tolbutamides are the stimulators of insulin release.

Insulin is destroyed by insulinase which sepa­rates the A and B chain of it. Peptidases also play a part in the destruction of insulin.

2. Adrenocortical Hormones:

The adrenalectomized animal exhibits the fol­lowing changes in carbohydrate metabolism:

a. Decrease in liver glycogen.

b. Less marked decrease in muscle glycogen.

c. Hypoglycemia.

d. Decreased intestinal absorption of glu­cose.

The changes are prevented by glucocorticoids. The glucocorticoid hormones release gluconeo­genic precursors, such as amino acids, from mus­cle. The hormones also release FFA from adipose tissue, resulting in inhibition of hepatic glycoly­sis. The increase in FFA in the liver results in an increase of acetyl-CoA which activates pyruvate carboxylase and so stimulates gluconeogenesis.

3.Anterior Pituitary Factors:

Growth hormone produces the following changes in carbohydrate metabolism:

a. Hyperglycemia and aggravation of diabe­tes in depancreatized animals.

b. Inhibition of insulin action with decreased utilization of carbohydrate and lowering of the respiratory quotient.

c. Diminution of the breakdown of muscle protein.

d. Increase in the mobilization of fat in the form of FFA from adipose tissue with the increase in lipase activity. The increase in FFA, and its use as the source of energy results in the excessive production of ke­tone bodies.

e. ACTH enhances the release of free fatty acids from adipose tissue and inhibits glu­cose utilization. It causes increase in blood sugar level by stimulating the secretion of adrenal cortex hormones.

4. Epinephrine:

a. Causes an increase in blood sugar and in blood lactate due to the acceleration of glycogenolysis in the liver and muscles.

b. Diminishes the uptake of glucose by tis­sue cells, thus interfering with its utiliza­tion.

c. Causes diminution in the amount of insu­lin released from the pancreas.

5.Thyroid Hormone:

a. Thyroxine accelerates hepatic glycogeno­lysis with consequent rise in blood sugar. This is due to increased sensitivity to epinephrine.

b. Thyroxine also increases the rate of ab­sorption of hexoses from the intestine and accelerates gluconeogenesis.

c. It has diabetogenic action.

6.Glucagon:

a. Promotes glycogenolysis in liver stimu­lating phosphorylase via cyclic AMP.

b. Causes breakdown of glycogen to lactic acid in muscle. The lactic acid is again converted to glucose by “Cori Cycle”.

c. Stimulates gluconeogenesis in liver.

7.Sex Hormones:

Estrogens stimulate increased insulin secretion and thus reduce blood sugar level. Testosterone also decreases blood sugar level.