Department of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, Ohio 45237, USA.
Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):315-21. doi: 10.1097/MCO.0b013e3283476e74.
To review our current understanding of the relationship between absorption of nutrients and intestinal inflammatory response.
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.
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.
回顾我们目前对营养物质吸收与肠道炎症反应之间关系的理解。
越来越多的证据表明肠道局部炎症事件与营养素的摄入有关。我们最近的研究使用清醒淋巴瘘大鼠模型表明，脂肪吸收会激活肠道黏膜肥大细胞。这伴随着肠道肥大细胞介质包括组胺、大鼠黏膜肥大细胞蛋白酶 II（RMCPII）以及脂质介质前列腺素 D2（PGD2）在淋巴中的释放显著增加。临床研究表明，动物脂肪摄入的增加可能在炎症性肠病的发病机制中起作用。这种饮食脂肪的影响不仅限于肠道，还可能扩展到全身。有证据表明高脂肪饮食引起的代谢综合征与低度慢性炎症状态有关。在这篇综述中，我们希望让读者相信脂肪吸收会产生深远的生理和病理生理后果。
了解营养物质吸收与肠道炎症之间的关系很重要。我们需要更好地理解营养物质吸收和肠道炎症反应中肠上皮细胞与肠道免疫细胞之间的相互作用。
