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迄今为止葡萄糖在小肠黏膜的吸收机制已被系统地阐明和接受,即经典的钠葡萄糖同向转运体(SGLT1)介导的主动转运机制。此外,当肠腔葡萄糖浓度高于SGLT1的转运饱和度时,葡萄糖转运蛋白2(GluT2)可能一过性易位于小肠黏膜上皮细胞顶膜来参与葡萄糖的异化扩散吸收,但小肠黏膜上皮细胞葡萄糖吸收的调节机制仍然不是完全清楚。近年来钙离子通道(CRAC)及细胞内钙信号对葡萄糖的吸收调节作用备受关注,二者可通过调节肠道葡萄糖转运体SGLT1和GluT2的表达及功能来调节小肠葡萄糖的吸收。本文以CRAC及细胞内钙信号对小肠黏膜上皮细胞葡萄糖的吸收调节作用及其分子机制进行论述,希望能为肥胖及其相关疾病的防治提供新的视野及潜在的新药研发靶点。
Up to now, the absorption mechanism of glucose in the intestinal mucosa has been systematically elucidated and accepted, that is, the active transport mechanism mediated by the classical sodium glucose-symporter (SGLT1). In addition, when the intestinal glucose concentration is higher than that of SGLT1, glucose transporter 2 (GluT2) may transiently localize on the apical membrane of intestinal mucosal epithelial cells to participate in the dissimilatory diffusion of glucose absorption, but the intestinal mucosal epithelial cell glucose uptake The regulatory mechanism is still not entirely clear. In recent years, attention has been paid to the regulation of glucose uptake by calcium channel (CRAC) and intracellular calcium signaling. Both of them regulate the intestinal glucose uptake by regulating the expression and function of intestinal glucose transporters SGLT1 and GluT2. In this paper, CRAC and intracellular calcium signaling on the absorption of small intestinal mucosal epithelial cells glucose regulation and molecular mechanisms discussed in the hope that the prevention and treatment of obesity and related diseases provide a new horizons and potential new drug development targets.