Gut microbiota and energy balance: role in obesity
Gut microbiota and energy balance: role in obesity
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DOI：
10.1017/s0029665114001700
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发表时间：
2015-08-01
影响因子：
7
通讯作者：
Blaut, Michael
中科院分区：
文献类型：
--
作者：
Blaut, Michael
人类消化道中的微生物群落与肥胖、糖尿病和肝病的发生有关。关于肠道微生物区系如何促进肥胖和代谢性疾病的拟议机制包括：(1)通过将膳食纤维转化为SCFA来改善饮食中的能量提取；(2)增加肠道对细菌脂多糖(LPS)的通透性，以应对高脂肪饮食的消耗，从而导致全身LPS水平升高和低级别炎症。动物研究表明，可发酵和不可发酵膳食纤维的生理效应不同，可发酵膳食纤维的长期和短期影响也不同。人体肠道微生物组富含与难消化的多糖降解有关的基因。膳食纤维的发酵程度和形成的摩尔比SCFA取决于它们的物理化学性质和单个微生物群。醋酸盐和丙酸在脂肪和葡萄糖代谢中起着重要作用。醋酸盐是肝脏新生脂肪生成的底物，而丙酸可用于糖异生。可发酵的膳食纤维转化为SCFA为宿主提供了额外的能量，这可能会促进肥胖。然而，流行病学研究表明，富含纤维的饮食是预防而不是促进肥胖的发展。这可能是因为SCFA也是游离脂肪酸受体(FFAR)的配体。FFAR的激活导致肠内分泌激素的表达和分泌增加，如导致饱腹感的胰高血糖素样肽1或YY肽。综上所述，SCFA在宿主能量平衡中的作用需要重新评估。
The microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long-and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an important role in lipid and glucose metabolism. Acetate serves as a substrate for de novo lipogenesis in liver, whereas propionate can be utilised for gluconeogenesis. The conversion of fermentable dietary fibre to SCFA provides additional energy to the host which could promote obesity. However, epidemiologic studies indicate that diets rich in fibre rather prevent than promote obesity development. This may be due to the fact that SCFA are also ligands of free fatty acid receptors (FFAR). Activation of FFAR leads to an increased expression and secretion of enteroendocrine hormones such as glucagon-like-peptide 1 or peptide YY which cause satiety. In conclusion, the role of SCFA in host energy balance needs to be re-evaluated.