PMID: 6161068Jan 1, 1980Paper

Carbohydrate metabolism and the glucoreceptor mechanism

Hormone and Metabolic Research. Supplement Series
S J AshcroftI H Williams

Abstract

Current views on the recognition of sugars as signals for insulin biosynthesis and release are discussed. Evidence is presented that the initial steps in the metabolism of N-acetyl-glucosamine differ from those in glucose metabolism in that for the former transport into the islet represents the rate-limiting step. Different enzymes phosphorylate these two sugar, but it is suggested that N-acetylglucosamine and glucose enter the beta-cell via the same carrier since 3-O-methylglucose is shown to be a competitive inhibitor of N-acetylglucosamine oxidation. Inhibitory effects on N-acetylglucosamine oxidation are also observed with caffeine, 3-isobutyl-methylxanthine and phloretin. Inhibition of N-acetylglucosamine metabolism is associated with inhibition of N-acetylglucosamine-stimulated insulin release and biosynthesis. Methylxanthines also inhibit uptake of 45Ca2+ by islet mitochondria. The possible physiological role of islet mitochondrial Ca2+ uptake in the regulation of beta-cell cytosolic Ca2+ concentration is discussed.

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