The Influence of the Endocrine Glands on Fatty Acid and Ketone Body Metabolism

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Abstract
Current concepts of intermediary fat metabolism and ketogenesis have been reviewed. The mechanisms involved in the ketosis of diabetes mellitus, fasting and insulin hypoglycemia and the antiketogenic action of glucose and insulin are discussed. In addition, the possible roles of the endocrine glands in fasting and insulin hypoglycemia ketosis are reviewed. Neither the adrenal medulla, the adrenal cortex or hypophysis are essential to the development of ketosis during fasting or hypoglycemia. Glucocorticoids suppress the ketosis resulting from fasting, cold-stress and fluoroacetate poisoning but not that due to insulin hypoglycemia or ketogenic pituitary extracts. Growth hormone, thyrotropin and corticotropin possess ketogenic and adipokinetic action, the latter independent of the adrenal cortices. The significance of multiple ketogenic factors and their possible modes of action are considered. The hypophysectomized rat develops greater ketosis and more hypoglycemia than does the normal rat during a seven-day fast.