The Glucoreceptor Mechanism in the Pancreatic Beta-Cell

Authors:
Open Access
Publisher website
Google Scholar
Abstract
Recent experimental contributions concerning the nature of the glucoreceptor mechanism in the B-cell are reviewed. The relative aptitude of different hexoses (glucose, mannose, fructose, galactose) to affect various parameters of islet function (insulin biosynthesis, calcium uptake, insulin release, ability to support the insulinotropic action of theophylline) does not support the view that a receptor molecule can be activated by unmetabolized sugars. The specific inhibition by mannoheptulose and other metabolic inhibitors of the stimulant action of glucose upon these various parameters rather indicates that the glucoreceptor mechanism for both insulin biosynthesis and release is dependent on a pathway of glucose metabolism in the B-cell. The accumulation of calcium in the cytosol of the B-cell represents a selective requirement for the releasing process, and apparently does not affect the glucoreceptor mechanism. The influence of alkali cations (Na+, K+, Li+, Tris) upon the various parameters of insular function suggests that the glucoreceptor mechanism for both insulin biosynthesis and release involves a sodium-sensitive step of glucose handling by the B-cell. Agents known to act upon the B-cell microtubular-microfilamentous system modify the secretory responsiveness to glucose, probably by altering the sensitivity of microtubules and microfilaments to cytosolic calcium.

This publication has 17 references indexed in Scilit: