Ashcroft S J, Sugden M C, Williams I H
Horm Metab Res Suppl. 1980;Suppl 10:1-7.
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.
本文讨论了目前关于糖类作为胰岛素生物合成和释放信号的认识。有证据表明，N-乙酰葡糖胺代谢的初始步骤与葡萄糖代谢不同，前者进入胰岛的转运是限速步骤。不同的酶使这两种糖磷酸化，但由于3-O-甲基葡萄糖被证明是N-乙酰葡糖胺氧化的竞争性抑制剂，因此有人提出N-乙酰葡糖胺和葡萄糖通过同一载体进入β细胞。咖啡因、3-异丁基-甲基黄嘌呤和根皮素对N-乙酰葡糖胺氧化也有抑制作用。N-乙酰葡糖胺代谢的抑制与N-乙酰葡糖胺刺激的胰岛素释放和生物合成的抑制有关。甲基黄嘌呤还抑制胰岛线粒体对45Ca2+的摄取。本文讨论了胰岛线粒体Ca2+摄取在调节β细胞胞质Ca2+浓度中的可能生理作用。
