Orginal Publication Date
MCV/Q, Medical College of Virginia Quarterly
Much of the emphasis in the pathogenesis of diabetes mellitus has justifiably been placed on the endocrine gland, the pancreas. Extensive studies on the biosynthesis and release of insulin from the beta cell, bihormonal control of metabolism by insulin and glucagon, and more recently the role of somatostatin have attracted the attention of students of the subject; but considerable evidence exists to suggest at least some role of tissue resistance to insulin in the pathogenesis of this disorder. There have been many advocates for extra pancreatic factors causing diabetes. One of the first was Mirsky, who proposed that diabetes might be due to excessive amounts of hepatic insulinase, an enzyme which degrades insulin. Vallance-Owen suggested that a circulating insulin antagonist labeled synalbumin might be the cause of insulin resistance in diabetes. This factor was later shown to be an artifact. Others, such as Antoniades, proposed that insulin might circulate predominantly in a bound form in diabetic subjects and thus not exert full biologic activity.
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