Section of Digestive Diseases, Yale University, 300 Cedar Street, TAC S241, PO Box 208019, New Haven, CT 06520-8019, USA.
Nat Rev Gastroenterol Hepatol. 2013 Nov;10(11):637-44. doi: 10.1038/nrgastro.2013.146. Epub 2013 Aug 20.
The development of obesity and NAFLD is known to be determined by host genetics, diet and lack of exercise. In addition, the gut microbiota has been identified to influence the development of both obesity and NAFLD. Evidence for the role of the gut microbiota has been shown by preclinical studies of transfer of gut microbiota from lean and obese individuals, with the recipient developing the metabolic features of the donor. Many bidirectional interactions of the gut microbiota, including with food, bile and the intestinal epithelium, have been identified. These interactions might contribute to the distinct steps in the progression from lean to obese states, and to steatosis, steatohepatitis and eventually fibrosis. The predominant steps are efficient caloric extraction from the diet, intestinal epithelial damage and greater entry of bacterial components into the portal circulation. These steps result in activation of the innate immune system, liver inflammation and fibrosis. Fortunately, therapeutic interventions might not require a full understanding of these complex interactions. Although antibiotics are too unselective in their action, probiotics have shown efficacy in reversing obesity and NASH in experimental systems, and are under investigation in humans.
肥胖症和非酒精性脂肪性肝病的发展已知取决于宿主遗传、饮食和缺乏运动。此外，肠道微生物群已被确定会影响肥胖症和非酒精性脂肪性肝病的发展。从瘦人和肥胖个体转移肠道微生物群的临床前研究表明了肠道微生物群的作用证据，接受者会发展出供体的代谢特征。已经确定了肠道微生物群的许多双向相互作用，包括与食物、胆汁和肠上皮的相互作用。这些相互作用可能有助于从瘦到肥胖状态的进展以及脂肪变性、脂肪性肝炎和最终纤维化的不同步骤。主要步骤是从饮食中有效提取卡路里、肠上皮损伤和更多细菌成分进入门静脉循环。这些步骤导致先天免疫系统的激活、肝脏炎症和纤维化。幸运的是，治疗干预可能不需要完全了解这些复杂的相互作用。尽管抗生素的作用过于没有选择性，但益生菌在实验系统中已被证明能有效逆转肥胖症和 NASH，并且正在人类中进行研究。
