新发现的微生物群和肥胖之间的联系。

C. Chakraborti
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引用次数: 276

摘要

由于肥胖具有严重的病理作用,世界范围内对其致病因素的研究仍在继续。该领域的最新进展揭示了肠道微生物群的组成模式与肥胖的发生之间可能存在的关系。一些研究结果表明,短链脂肪酸(SCFAs,微生物诱导的发酵产物)和脂多糖(LPS,革兰氏阴性微生物的一个组成部分)在连接两者的过程中起着关键作用。虽然几种短链脂肪酸是作为微生物发酵产物产生的,但已经发现其中的三种,即丁酸盐、丙酸盐和醋酸盐与肥胖有明确的关系;虽然就个体而言,它们既不是纯粹的致肥性,也不是反致肥性。其中,丁酸盐和丙酸盐主要是抗肥胖的。丁酸盐虽然是结肠细胞的主要能量来源,但已被发现可以增加线粒体活性,防止代谢性内毒素血症,改善胰岛素敏感性,具有抗炎潜力,增加肠道屏障功能,并在不引起吞咽的情况下防止饮食引起的肥胖。丙酸已被发现抑制胆固醇合成,从而拮抗醋酸酯的胆固醇升高作用,并抑制脂肪细胞中抵抗素的表达。此外,已经发现这两种SCFAs通过刺激肠道厌氧性激素和增加瘦素的合成来调节体重。与丁酸盐和丙酸盐不同,乙酸盐可被人体吸收,但它作为肝脏和脂肪细胞脂肪生成的底物,具有更大的致肥潜能。高脂肪饮食增加了脂多糖的吸收,而脂多糖又被发现与代谢性内毒素血症和诱导炎症导致肥胖有关。多种相互独立和相互关联的机制参与了这种联系过程,本文将讨论这些机制以及预防体重增加和肥胖的一些可能的补救措施。
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New-found link between microbiota and obesity.
Due to the grave pathological role of obesity, worldwide research is being continued to find out the causative factors involved in it. Recent advances in this field reveal a possible relationship between the compositional pattern of gut microbiota and genesis of obesity. Several study results have shown that short-chain fatty acids (SCFAs, microbiota-induced fermentation products) and lipopolysaccharides (LPS, an integral component of Gram negative microorganisms) play the key role in linking the two. Though several SCFAs are produced as microbiota-fermentation products, three of them, i.e., butyrate, propionate and acetate have been found to be definitely involved in obesity; though individually they are neither purely obesogenic nor antiobesogenic. Out of these, butyrate and propionate are predominantly antiobesogenic. Butyrate, though a major energy source for colonocytes, has been found to increase mitochondrial activity, prevent metabolic endotoxemia, improve insulin sensitivity, possess anti-inflammatory potential, increase intestinal barrier function and protect against diet-induced obesity without causing hypophagia. Propionate has been found to inhibit cholesterol synthesis, thereby antagonizing the cholesterol increasing action of acetate, and to inhibit the expression of resistin in adipocytes. Moreover, both these SCFAs have been found to cause weight regulation through their stimulatory effect on anorexigenic gut hormones and to increase the synthesis of leptin. Unlike butyrate and propionate, acetate, which is substantially absorbed, shows more obesogenic potential, as it acts as a substrate for hepatic and adipocyte lipogenesis. High fat diet increases the absorption of LPS, which, in turn, has been found to be associated with metabolic endotoxemia and to induce inflammation resulting in obesity. Multiple independent and interrelated mechanisms have been found to be involved in such linking processes which are discussed in this review work along with some possible remedial measures for prevention of weight gain and obesity.
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