THE ROLE OF THE ENDOCRINE GLANDS IN KETOSIS. II. KETONEMIA FOLLOWING INSULIN HYPOGLYCEMIA*

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Abstract
The role of the hypophysis and other endocrine glands in ketonemia during insulin hypoglycemia was studied in rats fasted for 24 hours. In intact rats insulin caused an initial decline in ketonemia followed by a rise 4 and 6 hours after insulin. Although previous administration of cortisone preserved abundant liver glycogen and suppressed fasting ketosis, it did not prevent post-insulin hypoglycemic ketosis. Liver glycogen was depleted in the latter instance. Insulin hypoglycemic ketosis also occurred in adrenalectomized, adrenal demedullated, hypophysectomized, and hypophysectomized-adrenalectomized rats. Adrenalectomized rats did not tolerate insulin hypoglycemia unless maintained on DCA. DCA was not necessary for fasting ketosis. Exact quantitative comparisons were inconclusive because of differing degrees of hypoglycemia and ignorance of the rates of ketogenesis and ketolysis. Treatment of hypophysectomized rats with triiodothyronine seemed to enhance the degree of ketonemia. Crystalline glucagon, treated to inactivate residual insulin, had no effect on insulin hypoglycemic ketosis while additional insulin decreased ketonemia. Epinephrine caused a rapid temporary decline in fasting ketosis. The hypophysis, adrenal medulla, and glucocorticoids of the adrenal cortex are not essential for the development of ketosis after insulin hypoglycemia. Suppression of endogenous insulin secretion probably plays an important role in the genesis of the ketosis.