Division of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, Yokohama, Kanagawa, 236-0004, Japan.
Semin Immunopathol. 2014 Jan;36(1):115-32. doi: 10.1007/s00281-013-0404-6. Epub 2013 Dec 14.
The recent rise in obesity-related diseases, such as nonalcoholic fatty liver disease and its strong association with microbiota, has elicited interest in the underlying mechanisms of these pathologies. Experimental models have highlighted several mechanisms connecting microbiota to the development of liver dysfunction in nonalcoholic steatohepatitis (NASH) such as increased energy harvesting from the diet, small intestine bacterial overgrowth, modulation of the intestinal barrier by glucagon-like peptide-2 secretions, activation of innate immunity through the lipopolysaccharide-CD14 axis caused by obesity-induced leptin, periodontitis, and sterile inflammation. The manipulation of microbiota through probiotics, prebiotics, antibiotics, and periodontitis treatment yields encouraging results for the treatment of obesity, diabetes, and NASH, but data in humans is scarce.
近年来，与肥胖相关的疾病（如非酒精性脂肪性肝病及其与微生物组的密切关联）不断增加，这引起了人们对这些疾病潜在机制的关注。实验模型突出了几种将微生物组与非酒精性脂肪性肝炎（NASH）中肝功能障碍的发展联系起来的机制，例如从饮食中获取更多的能量、小肠细菌过度生长、胰高血糖素样肽-2 分泌对肠道屏障的调节、肥胖引起的瘦素导致的脂多糖-CD14 轴对固有免疫的激活、牙周炎和无菌性炎症。通过益生菌、益生元、抗生素和牙周炎治疗来操纵微生物组，为肥胖、糖尿病和 NASH 的治疗带来了可喜的结果，但人类的数据还很缺乏。
