Department of Cell and Molecular Physiology, Center for Gastrointestinal Biology and Disease University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7574, USA.
Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):328-33. doi: 10.1097/MCO.0b013e3283478727.
To highlight recent evidence supporting a concept that intestinal inflammation is a mediator or contributor to development of obesity and insulin resistance.
Current views suggest that obesity-associated systemic and adipose tissue inflammation promote insulin resistance, which underlies many obesity-linked health risks. Diet-induced changes in gut microbiota also contribute to obesity. Recent findings support a concept that high-fat diet and bacteria interact to promote early inflammatory changes in the small intestine that contribute to development of or susceptibility to obesity and insulin resistance. This review summarizes the evidence supporting a role of intestinal inflammation in diet-induced obesity and insulin resistance and discusses mechanisms.
The role of diet-induced intestinal inflammation as an early biomarker and mediator of obesity, and insulin resistance warrants further study.
强调近期支持肠道炎症是肥胖和胰岛素抵抗发展的介质或促成因素的证据。
目前的观点表明，肥胖相关的全身和脂肪组织炎症会促进胰岛素抵抗，这是许多与肥胖相关的健康风险的基础。饮食引起的肠道菌群变化也会导致肥胖。最近的研究结果支持这样一种观点，即高脂肪饮食和细菌相互作用，促进小肠的早期炎症变化，从而导致肥胖和胰岛素抵抗的发生或易感性。本综述总结了支持肠道炎症在饮食诱导的肥胖和胰岛素抵抗中的作用的证据，并讨论了相关机制。
饮食诱导的肠道炎症作为肥胖和胰岛素抵抗的早期生物标志物和介质的作用值得进一步研究。
