The effects of insulin and glucocorticoids on carbohydrate, fat and protein metabolism of various isolated tissues have been summarized. Insulin is required for maximum glucose utilization by liver, muscle and adipose tissue, but is not required by the brain and nervous tissue. Glucocorticoids do not oppose or antagonize the primary effect of insulin which is to increase the permeability of cells to glucose. However, glucose phosphorylation by muscle is decreased by the presence of pituitary and adrenal cortical hormones in the absence of insulin.
Insulin and the glucocorticoids do appear to play opposing roles in the mobilization of fatty acids (FFA). Many hormones promote FFA release from adipose tissue; however, the full lipolytic effect is not achieved in the absence of the adrenal cortex. Insulin, on the other hand, inhibits the lipolytic effect of catecholamines, glucagon, and ACTH.
Ketosis is not observed in experimental diabetes if FFA mobilization is prevented by removal of the adrenals or pituitary. On the other hand, mobilization of FFA does not lead to ketosis if adequate insulin is available. An important aspect of glucocorticoid action in diabetes is probably in the area of FFA mobilization and ketone body production. However, the role of the adrenal cortex in protein catabolism and gluconeogenesis is of equal concern. Overproduction as well as under-utilization of glucose remains the central problem in attempting to regulate the diabetic patient.