Diabetes Mellitus - A Disorder of Cellular Information Transmission?

Abstract

On the basis of available data it is suggested that the glucose induced rapid insulin discharge from the pancreatic β-cell is not a direct consequence of glucose metabolism in the β-cell but is evoked by activation of adenyl cyclase by glucose per se. Glucose thereby acts as a trigger of a signal chain connecting a glucose receptor, over adenyl cyclase and cyclic AMP, with the insulin releasing machinery. The metabolism of glucose in the β-cell may participate in the process of insulin release by modulating the signal chain via various factors (glucose metabolites, availability of energy and calcium etc.). It is suggested that the defective insulin discharge in diabetes and prediabetes is caused by a selective impairment of the glucose receptor of the β-cell leading to inability of the cell to recognize hyperglycemia as a stimulator of adenyl cyclase activity.