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Dietary excess regulates absorption and surface of gut epithelium through intestinal PPARα
Nature Communications ( IF 16.6 ) Pub Date : 2021-12-02 , DOI: 10.1038/s41467-021-27133-7
Ozren Stojanović 1, 2, 3 , Jordi Altirriba 1 , Dorothée Rigo 1, 2 , Martina Spiljar 1, 2 , Emilien Evrard 1 , Benedek Roska 1 , Salvatore Fabbiano 1, 2 , Nicola Zamboni 4 , Pierre Maechler 1, 2 , Françoise Rohner-Jeanrenaud 1 , Mirko Trajkovski 1, 2
Affiliation  

Intestinal surface changes in size and function, but what propels these alterations and what are their metabolic consequences is unknown. Here we report that the food amount is a positive determinant of the gut surface area contributing to an increased absorptive function, reversible by reducing daily food. While several upregulated intestinal energetic pathways are dispensable, the intestinal PPARα is instead necessary for the genetic and environment overeating–induced increase of the gut absorptive capacity. In presence of dietary lipids, intestinal PPARα knock-out or its pharmacological antagonism suppress intestinal crypt expansion and shorten villi in mice and in human intestinal biopsies, diminishing the postprandial triglyceride transport and nutrient uptake. Intestinal PPARα ablation limits systemic lipid absorption and restricts lipid droplet expansion and PLIN2 levels, critical for droplet formation. This improves the lipid metabolism, and reduces body adiposity and liver steatosis, suggesting an alternative target for treating obesity.



中文翻译:

饮食过量通过肠道 PPARα 调节肠道上皮细胞的吸收和表面

肠表面的大小和功能发生变化,但推动这些变化的因素及其代谢后果是什么尚不清楚。在这里,我们报告食物量是肠道表面积的积极决定因素,有助于增加吸收功能,可通过减少日常食物来逆转。虽然一些上调的肠道能量通路是可有可无的,但肠道 PPARα 对于遗传和环境暴饮暴食引起的肠道吸收能力增加是必需的。在存在膳食脂质的情况下,肠道 PPARα 敲除或其药理学拮抗作用可抑制小鼠和人体肠道活组织检查中的肠隐窝扩张并缩短绒毛,从而减少餐后甘油三酯的转运和营养摄取。肠道 PPARα 消融限制全身脂质吸收并限制脂滴扩张和 PLIN2 水平,这对液滴形成至关重要。这改善了脂质代谢,并减少了身体肥胖和肝脏脂肪变性,表明了治疗肥胖症的替代目标。

更新日期:2021-12-02
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