Gradenigo Hospital, Turin, Italy.
Curr Opin Lipidol. 2010 Feb;21(1):76-83. doi: 10.1097/MOL.0b013e3283347ebb.
To examine the role of gut microbiota in the regulation of host energy homeostasis and its role in the pathogenesis of obesity, diabetes and nonalcoholic fatty liver disease (NAFLD).
Experimental models highlight several mechanisms connecting gut microbiota to host energy metabolism: increased energy harvesting from the diet, regulation of appetite through gut peptide, secretion, regulation of tissue-free fatty acid composition and uptake, storage and oxidation, modulation of intestinal barrier by glucagon-like peptide-2 secretion, activation of innate immunity and hepatic fibrogenesis through the lipopolysaccharide (LPS)-toll-like receptor-4 axis.Gut microbiota manipulation through antibiotics, prebiotics and probiotics yields encouraging results for the treatment of obesity, diabetes and NAFLD in animal models, but data in humans are currently scarce.
Gut microbiota manipulation yielded encouraging results for the treatment of different metabolic disorders in experimental models. However, changing intestinal microbiota may be more difficult in free-living individuals compared to standardized laboratory models, and its long-term consequences are unknown. To safely and effectively change human gut microflora, future research should highlight the complex hormonal, immunomodulatory and metabolic mechanisms underlying microbiota-host interactions in different tissues and candidate treatments should be evaluated in well designed trials with patient-oriented end-points.
探讨肠道微生物群在宿主能量稳态调节及其在肥胖症、糖尿病和非酒精性脂肪性肝病（NAFLD）发病机制中的作用。
实验模型强调了几种将肠道微生物群与宿主能量代谢联系起来的机制：从饮食中增加能量摄取、通过肠肽调节食欲、分泌、调节组织游离脂肪酸组成和摄取、储存和氧化、通过胰高血糖素样肽-2 分泌调节肠道屏障、通过脂多糖（LPS）-toll 样受体-4 轴激活先天免疫和肝纤维化。通过抗生素、益生元和益生菌对肠道微生物群进行操纵，为肥胖症、糖尿病和 NAFLD 的动物模型治疗带来了可喜的结果，但目前人类的数据还很缺乏。
肠道微生物群的操纵为治疗不同的代谢紊乱提供了实验模型中令人鼓舞的结果。然而，与标准化的实验室模型相比，改变自由生活个体的肠道微生物群可能更加困难，其长期后果尚不清楚。为了安全有效地改变人类肠道菌群，未来的研究应强调微生物群与宿主相互作用在不同组织中的复杂激素、免疫调节和代谢机制，候选治疗方法应在具有患者导向终点的精心设计的试验中进行评估。
