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The Physiology of Insulin Release

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Abstract

The β cells of the islets of Langerhans play a primary role in the pathogenesis of diabetes mellitus in man. Several lines of evidence obtained from clinical studies on diabetic subjects support this statement. Tolbutamide is an oral hypoglycemic agent which has been shown to stimulate insulin release from the β cell and to maintain normoglycemia in certain diabetic subjects. Thus tolbutamide apparently stimulates insulin secretion more effectively than glucose in these patients, which would suggest an impairment in glucose-induced insulin release in the β cells. Detailed studies on the pattern and rate of glucose-induced insulin secretion in maturity-onset diabetes and early stages of juvenile diabetes have shown a delay in the response of the β cells to glucose stimulation.1 These findings also indicate an impairment in the ability of the β cell to recognize glucose and to translate this recognition into the release of insulin. Transplantation of the whole pancreas has been accomplished in diabetic patients.2–4 During the period of survival of the transplant, the patients became normoglycemic and did not require exogenous insulin therapy, which clearly indicates that the primary defect is in the islet cells of the diabetic. The ultimate quest is to establish the identity of the defect or defects present in the β cells of diabetics. In order to search for these possible abnormalities, it is essential that basic information be obtained on the normal mechanisms for the formation, storage, and release of insulin by β cells. This chapter will be devoted to a review of the information available on the basic mechanism of insulin secretion as well as indicating potential sites for defects in this mechanism in diabetes mellitus.

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Lacy, P.E. (1977). The Physiology of Insulin Release. In: Volk, B.W., Wellmann, K.F. (eds) The Diabetic Pancreas. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2325-9_8

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