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首页> 外文期刊>American Journal of Physiology >Intestinal adaptation and Reg gene expression induced by antidiabetic duodenal-jejunal bypass surgery in Zucker fatty rats
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Intestinal adaptation and Reg gene expression induced by antidiabetic duodenal-jejunal bypass surgery in Zucker fatty rats

机译：Zucker肥胖大鼠抗糖尿病十二指肠-空肠旁路手术诱导的肠道适应和Reg基因表达

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摘要

The antidiabetic mechanism of bariatric surgery includes specific changes in the secretion of incretins. To identify additional players originating from the gut, we evaluated the effects of duodenal-jejunal bypass (DJB) in morbidly obese Zucker fatty rats. A fast relief of hyperglycemia and hyperinsulinemia was achieved even before a significant weight loss occurred. Fourteen days after DJB, we characterized the changes in intestinal histochemistry in the bypassed duodenum and shortcut jejunum that was reanastomosed directly to the starting point of the duodenum and compared with the corresponding regions of sham-operated rats. The bypassed duodenum exhibited mucosal atrophy and apoptosis and decreased proliferative renewal. In shortcut jejunum, DJB resulted in 40% significantly enlarged intestinal circumference and increased epithelial proliferation, especially in putative transit-amplifying (TA) cells and the crypt. Because Reg family proteins promote cell growth and survival, we explored their expression in the intestine. With the use of immunohistochemistry, Reg1, -3α, and -3β were normally expressed in intestinal mucosa. After DJB, the level of Reg1 protein was reduced, whereas Reg3α and -3β were not changed in bypassed duodenum. Downstream in shortcut jejunum, the levels of Reg1 and -3β were greatly induced and especially concentrated in the putative TA cells. Our results revealed significant changes in the integrity and proliferation of the intestinal mucosa as a consequence of DJB, and in cell- and isoform-specific expression of Reg proteins within the replicating mucosal epithelium, and provide evidence indicating that the activation of Reg proteins may contribute to intestinal compensation against increased load and/or to improving insulin sensitivity.
机译：减肥手术的抗糖尿病机制包括肠降血糖素分泌的特定变化。为了确定来自肠道的其他参与者，我们评估了十二指肠-空肠旁路（DJB）在病态肥胖的祖克肥胖大鼠中的作用。即使在未出现明显的体重减轻之前，也可以快速缓解高血糖和高胰岛素血症。 DJB后十四天，我们表征了绕过的十二指肠和空肠空肠的肠道组织化学变化，这些肠十二指肠和空肠直接重新吻合到十二指肠起点，并与假手术大鼠的相应区域进行了比较。绕过的十二指肠表现出粘膜萎缩和凋亡，并减少了增殖更新。在捷径空肠中，DJB导致40％的肠道周长显着增大，并增加上皮增殖，特别是在假定的转运放大（TA）细胞和隐窝中。由于Reg家族蛋白可促进细胞生长和存活，因此我们探索了它们在肠中的表达。通过使用免疫组织化学，Reg1，-3α和-3β通常在肠粘膜中表达。 DJB后，旁路十二指肠中Reg1蛋白的水平降低，而Reg3α和-3β不变。在空肠空肠的下游，Reg1和-3β的水平被大大诱导，尤其集中在假定的TA细胞中。我们的研究结果表明，DJB可导致肠道粘膜的完整性和增殖发生显着变化，以及在复制的粘膜上皮中Reg蛋白的细胞和同工型特异性表达，并提供证据表明Reg蛋白的激活可能有助于肠道补偿以增加负荷和/或改善胰岛素敏感性。

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