GH alters carbohydrate metabolism. Many of its actions may be secondary to increased fat mobilization and oxidation. (Remember, an increase in serum free fatty acids inhibits uptake of glucose in skeletal muscle and adipose tissue.) After administration of GH, blood glucose rises. The hyperglycemic effects of GH are mild and slower than those of glucagon and epinephrine. The increase in blood glucose results in part from decreased glucose uptake and use in skeletal muscle and adipose tissue. Liver glucose output increases, and this is probably not a result of glycogenolysis. In fact, glycogen levels can rise after administration of GH. However, the increase in fatty acid oxidation and hence the rise in liver acetyl coenzyme A (acetyl CoA) stimulate gluconeogenesis, followed by increased glucose production from substrates such as lactate and glycerol.
GH alters carbohydrate metabolism. Many of its actions may be secondary to increased fat mobilization and oxidation. (Remember, an increase in serum free fatty acids inhibits uptake of glucose in skeletal muscle and adipose tissue.) After administration of GH, blood glucose rises. The hyperglycemic effects of GH are mild and slower than those of glucagon and epinephrine. The increase in blood glucose results in part from decreased glucose uptake and use in skeletal muscle and adipose tissue. Liver glucose output increases, and this is probably not a result of glycogenolysis. In fact, glycogen levels can rise after administration of GH. However, the increase in fatty acid oxidation and hence the rise in liver acetyl coenzyme A (acetyl CoA) stimulate gluconeogenesis, followed by increased glucose production from substrates such as lactate and glycerol.
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