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首页> 外文期刊>American Journal of Physiology >Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome.
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Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome.

机译：在实验性短肠综合征中，营养素刺激的GLP-2释放和隐窝细胞增殖。

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摘要

Glucagon-like peptide-2 (GLP-2) is an enteroendocrine peptide that is released in response to luminal nutrients and has unique trophic actions in the gastrointestinal tract. These features suggest GLP-2 may be important in controlling intestinal adaptation. We examined the relationship over time of GLP-2 production and adaptation to intestinal resection, the effects of resection-induced malabsorption on GLP-2 production, and the correlation of endogenous serum GLP-2 levels with adaptation as measured by crypt-cell proliferation (CCP). We initially examined the effect of nutrient malabsorption, induced by a 90% resection of the proximal intestine studied on day 4, on the time course and levels of GLP-2 release. Secondly, the degree of malabsorption was varied by performing intestinal transection or 50, 75, or 90% resection of proximal small intestine. Finally, the relationship of GLP-2 levels over time with adaptation to a 90% resection was examined by determining GLP-2 levels on days 7, 14, and 28, andcorrelating this with intestinal adaptation, as assessed by morphology and CCP rate. A 90% resection significantly increased basal and postprandial GLP-2 levels, with a net increase in nutrient-stimulated exposure over 90 min; GLP-2 exposure (integrated levels vs. time) increased 12.7-fold in resected animals (P < 0.001). Basal and postprandial GLP-2 levels significantly correlated with the magnitude of intestinal resection (r(2) = 0.71; P < 0.001), CCP (r(2) = 0.48; P < 0.005), and nutrient malabsorption (protein, P < 0.001; fat, P < 0.005). The increase in CCP was maintained to 28 days after small bowel resection and was associated with an ongoing elevation in GLP-2 release. These findings suggest that GLP-2 is important in initiating and maintaining the small intestinal adaptive response to resection.
机译：胰高血糖素样肽2（GLP-2）是一种肠内分泌肽，可响应腔内营养而释放，并在胃肠道中具有独特的营养作用。这些特征表明GLP-2可能在控制肠适应中很重要。我们研究了随着时间的推移GLP-2产生和适应于肠切除的关系，切除引起的吸收不良对GLP-2产生的影响以及内源性血清GLP-2水平与隐窝细胞增殖所测量的适应性之间的相关性（ CCP）。我们最初检查了在第4天研究的近端肠切除90％引起的营养吸收不良对时间进程和GLP-2释放水平的影响。其次，吸收不良的程度可通过进行肠横切或近端小肠切除50％，75％或90％来改变。最后，通过确定第7、14、28天的GLP-2水平并将其与肠道适应性相关联（通过形态学和CCP率评估），研究了GLP-2水平随时间变化与适应90％切除的关系。 90％的切除显着增加了基础和餐后GLP-2的水平，在90分钟内营养刺激的暴露量净增加;在切除的动物中，GLP-2的暴​​露量（相对于时间的综合水平）增加了12.7倍（P <0.001）。基底和餐后GLP-2水平与肠切除的大小（r（2）= 0.71; P <0.001），CCP（r（2）= 0.48; P <0.005）和营养吸收不良（蛋白质，P < 0.001;脂肪，P <0.005）。小肠切除后，CCP的增加一直维持到28天，并且与GLP-2释放的持续升高有关。这些发现表明，GLP-2在启动和维持对切除的小肠适应性反应中很重要。

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