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Nutrient-induced inflammation in the intestine.

机译:营养物引起的肠道炎症。

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摘要

PURPOSE OF REVIEW: To review our current understanding of the relationship between absorption of nutrients and intestinal inflammatory response. RECENT FINDINGS: There is increasing evidence linking gut local inflammatory events with the intake of nutrients. Our recent studies, using the conscious lymph fistula rat model, demonstrate that fat absorption activates the intestinal mucosal mast cells. This is accompanied by a dramatic increase in the lymphatic release of mast cell mediators including histamine, rat mucosal mast cell protease II (RMCPII), as well as the lipid mediator prostaglandin D2 (PGD2). Clinical studies suggest that increased consumption of animal fat may play a role in the pathogenesis of inflammatory bowel disease. This impact of dietary fat may not be restricted to the gut but may extend to the whole body. There is evidence linking a high-fat diet-induced metabolic syndrome, with a low-grade chronic inflammatory state. In this review, we hope to convince the readers that fat absorption can have far reaching physiological and pathophysiological consequences. SUMMARY: Understanding the relationship between nutrient absorption and intestinal inflammation is important. We need a better understanding of the interaction between enterocytes and the intestinal immune cells in nutrient absorption and the gut inflammatory responses.
机译:审查的目的:审查我们目前对营养吸收与肠道炎症反应之间关系的理解。最近的发现:越来越多的证据表明肠道局部炎症事件与营养摄入有关。我们最近的研究使用有意识的淋巴瘘大鼠模型,证明脂肪吸收激活肠粘膜肥大细胞。这伴随着肥大细胞介质包括组胺,大鼠粘膜肥大细胞蛋白酶II(RMCPII)以及脂质介质前列腺素D2(PGD2)的淋巴释放急剧增加。临床研究表明,动物脂肪的消耗增加可能在炎症性肠病的发病机理中起作用。饮食脂肪的这种影响可能不仅限于肠道,还可能扩展到整个身体。有证据表明,高脂饮食诱发的代谢综合征与低度慢性炎症状态有关。在这篇综述中,我们希望使读者相信脂肪吸收会产生深远的生理和病理生理后果。摘要:了解营养吸收与肠道炎症之间的关系很重要。我们需要更好地了解肠上皮细胞和肠道免疫细胞之间在营养吸收和肠道炎症反应中的相互作用。

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