Estriol blunts postprandial blood glucose rise in male rats through regulating intestinal glucose transporters.
Estriol blunts postprandial blood glucose rise in male rats through regulating intestinal glucose transporters.
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雌三醇通过调节肠道葡萄糖转运蛋白来抑制雄性大鼠餐后血糖升高。
DOI：
10.1152/ajpendo.00209.2013
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Zhu,BaoTing
中科院分区：
文献类型：
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作者：
Yamabe,Noriko;Kang,KiSung;Lee,Woojung;Kim,Su-Nam;Zhu,BaoTing
尽管健康的晚期妊娠女性的总食物摄入量增加，但其餐后血糖峰值水平通常远低于健康非妊娠女性的水平。在这项研究中，我们试图确定是否雌三醇（E3），主要是在人类怀孕期间产生的内源性雌激素，有助于调节健康正常大鼠的餐后血糖水平。大鼠体内研究表明，口服葡萄糖给药后，E3减弱了血糖升高的速度和幅度，但似乎不影响葡萄糖吸收的总量。E3也不影响胰岛素分泌，但与溶剂处理的动物相比，它显著降低了肠道葡萄糖转运速率。与这一发现相一致，钠依赖性葡萄糖转运蛋白1和2的表达显着下调E3治疗的刷状缘膜和基底外侧膜，分别肠细胞。大多数观察到的体内效应与E3相比明显强于17β-雌二醇。利用分化的人Caco-2肠上皮细胞单层培养作为体外模型，我们证实生理相关浓度的E3可以通过抑制葡萄糖转运蛋白2的表达直接抑制葡萄糖摄取，而17β-雌二醇没有类似的作用。以上结果表明，E3可通过调节肠道葡萄糖转运蛋白的水平来抑制大鼠餐后血糖峰。
Despite increased total food intake in healthy, late-stage pregnant women, their peak postprandial blood sugar levels are normally much lower than the levels seen in healthy nonpregnant women. In this study, we sought to determine whether estriol (E3), an endogenous estrogen predominantly produced during human pregnancy, contributes to the regulation of the postprandial blood glucose level in healthy normal rats. In vivo studies using rats showed that E3blunted the speed and magnitude of the blood glucose rise following oral glucose administration, but it did not appear to affect the total amount of glucose absorbed. E3also did not affect insulin secretion, but it significantly reduced the rate of intestinal glucose transport compared with vehicle-treated animals. Consistent with this finding, expression of the sodium-dependent glucose transporter 1 and 2 was significantly downregulated by E3treatment in the brush-border membrane and basolateral membrane, respectively, of enterocytes. Most of the observed in vivo effects were noticeably stronger with E3than with 17β-estradiol. Using differentiated human Caco-2 enterocyte monolayer culture as an in vitro model, we confirmed that E3at physiologically relevant concentrations could directly inhibit glucose uptake via suppression of glucose transporter 2 expression, whereas 17β-estradiol did not have a similar effect. Collectively, these data showed that E3can blunt the postprandial glycemic surge in rats through modulating the level of intestinal glucose transporters.