Resistant starch can improve insulin sensitivity independently of the gut microbiota.
Resistant starch can improve insulin sensitivity independently of the gut microbiota.
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DOI：
10.1186/s40168-017-0230-5
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发表时间：
2017-02-07
期刊：
影响因子：
15.5
通讯作者：
Ramer-Tait AE
中科院分区：
文献类型：
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作者：
Bindels LB;Segura Munoz RR;Gomes-Neto JC;Mutemberezi V;Martínez I;Salazar N;Cody EA;Quintero-Villegas MI;Kittana H;de Los Reyes-Gavilán CG;Schmaltz RJ;Muccioli GG;Walter J;Ramer-Tait AE
与肥胖有关的疾病，包括2型糖尿病和心血管疾病，在工业化国家已达到流行病的程度，因此，预防这些疾病的饮食干预措施很重要。抗性淀粉（RS）在临床试验中改善胰岛素敏感性，但这种健康益处的机制仍然知之甚少。由于肠道微生物群的RS发酵导致生理活性代谢物的形成，因此我们选择专门确定肠道微生物群在介导RS代谢益处中的作用。为了实现这一目标，我们确定了RS添加到西方饮食中对有和没有微生物群的小鼠的宿主代谢的影响。常规小鼠的RS喂养改善了胰岛素敏感性，并纠正了一些西方饮食诱导的微生物组组成变化。然而，在无菌同窝仔中进行的平行实验表明，RS介导的胰岛素水平改善也发生在没有微生物群的情况下。RS降低了脂肪组织巨噬细胞标志物的基因表达，并改变了无菌和常规小鼠中几种胆汁酸的盲肠浓度;这些效应与代谢益处密切相关，提供了一种潜在的微生物独立机制来解释RS的生理效应。这项研究表明，饮食RS产生的一些代谢益处，特别是胰岛素水平的改善，独立于微生物群发生，可能涉及胆汁酸循环和脂肪组织免疫调节的改变。这项工作也为未来的机制研究奠定了先例，旨在确定肠道微生物群在介导生物活性化合物和功能性食品的益处中的致病作用。本文的在线版本（doi：10.1186/s40168-017-0230-5）包含补充材料，可供授权用户使用。
Obesity-related diseases, including type 2 diabetes and cardiovascular disease, have reached epidemic proportions in industrialized nations, and dietary interventions for their prevention are therefore important. Resistant starches (RS) improve insulin sensitivity in clinical trials, but the mechanisms underlying this health benefit remain poorly understood. Because RS fermentation by the gut microbiota results in the formation of physiologically active metabolites, we chose to specifically determine the role of the gut microbiota in mediating the metabolic benefits of RS. To achieve this goal, we determined the effects of RS when added to a Western diet on host metabolism in mice with and without a microbiota. RS feeding of conventionalized mice improved insulin sensitivity and redressed some of the Western diet-induced changes in microbiome composition. However, parallel experiments in germ-free littermates revealed that RS-mediated improvements in insulin levels also occurred in the absence of a microbiota. RS reduced gene expression of adipose tissue macrophage markers and altered cecal concentrations of several bile acids in both germ-free and conventionalized mice; these effects were strongly correlated with the metabolic benefits, providing a potential microbiota-independent mechanism to explain the physiological effects of RS. This study demonstrated that some metabolic benefits exerted by dietary RS, especially improvements in insulin levels, occur independently of the microbiota and could involve alterations in the bile acid cycle and adipose tissue immune modulation. This work also sets a precedent for future mechanistic studies aimed at establishing the causative role of the gut microbiota in mediating the benefits of bioactive compounds and functional foods. The online version of this article (doi:10.1186/s40168-017-0230-5) contains supplementary material, which is available to authorized users.