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腾讯登录Nature：高饱和脂肪膳食导致菌群失调及结肠炎机制
| 导读 | 6月13日，<em>Nature</em>杂志在线报道了高饱和脂肪膳食导致人体菌群改变并诱发免疫性结肠炎研究的重要进展。由于某些新的对人类健康不利的环境因素的影响，在过去一个世纪里，西方人群的复合微生物组很可能已经发生了变化。
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本研究发现，高饱... |
6月13日，<em>Nature</em>杂志在线报道了高饱和脂肪膳食导致人体菌群改变并诱发免疫性结肠炎研究的重要进展。由于某些新的对人类健康不利的环境因素的影响，在过去一个世纪里，西方人群的复合微生物组很可能已经发生了变化。
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本研究发现，高饱和脂肪膳食（而非多不饱和脂肪），可改变微生物聚集的条件，并促进原本低丰度的亚硫酸盐还原菌，沃氏嗜胆菌的增殖。这一过程伴随着促炎症的T辅助细胞1型（TH1）免疫反应，以及结肠炎在遗传性易感的Il10-/-而非野生型小鼠体内的发病增加。
这些效应是由牛奶来源的脂肪触发的牛磺酸与肝胆汁酸的结合介导的。这增加了亚硫酸盐还原菌，如沃氏嗜胆菌（B. wadsworthia），的利用原材料有机硫的供应量。当小鼠被饲以低脂饲料并添加牛磺胆酸，而不是甘氨胆酸时，Il10-/-小鼠出现B. wadsworthia的激增和结肠炎。
总之，通过促进宿主胆汁酸成分的改变，膳食脂肪可显著改变肠道微生物的聚集条件，并导致可打破免疫稳态的生态失调。这些研究结果，为西方式的高饱和脂肪膳食如何增加复杂免疫性疾病（如炎症性肠道疾病）在遗传易感性宿主的发病率，提供了一个可能的解释。
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<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061419385765.jpg" alt="" width="113" height="149" border="0" hspace="0" />
<a title="" href="http://dx.doi.org/10.1016/j.cell.2011.10.017" target="_blank">doi:</a><a title="" href="http://dx.doi.org/10.1038/nature11225" target="_blank">10.1016/j.cell.2011.10.017</a>
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<br/><strong>Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice</strong><br/>
Suzanne Devkota,1 Yunwei Wang,1 Mark W. Musch,1 Vanessa Leone,1 Hannah Fehlner-Peach,1 Anuradha Nadimpalli,1 Dionysios A. Antonopoulos,2 Bana Jabri1 & Eugene B. Chang1
The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health1. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2. This was associated with a pro-inflammatory T helper type 1 (TH1) immune response and increased incidence of colitis in genetically susceptible Il10?/?, but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10?/? mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
<br/>来源：生物谷
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本研究发现，高饱和脂肪膳食（而非多不饱和脂肪），可改变微生物聚集的条件，并促进原本低丰度的亚硫酸盐还原菌，沃氏嗜胆菌的增殖。这一过程伴随着促炎症的T辅助细胞1型（TH1）免疫反应，以及结肠炎在遗传性易感的Il10-/-而非野生型小鼠体内的发病增加。
这些效应是由牛奶来源的脂肪触发的牛磺酸与肝胆汁酸的结合介导的。这增加了亚硫酸盐还原菌，如沃氏嗜胆菌（B. wadsworthia），的利用原材料有机硫的供应量。当小鼠被饲以低脂饲料并添加牛磺胆酸，而不是甘氨胆酸时，Il10-/-小鼠出现B. wadsworthia的激增和结肠炎。
总之，通过促进宿主胆汁酸成分的改变，膳食脂肪可显著改变肠道微生物的聚集条件，并导致可打破免疫稳态的生态失调。这些研究结果，为西方式的高饱和脂肪膳食如何增加复杂免疫性疾病（如炎症性肠道疾病）在遗传易感性宿主的发病率，提供了一个可能的解释。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061419385765.jpg" alt="" width="113" height="149" border="0" hspace="0" />
<a title="" href="http://dx.doi.org/10.1016/j.cell.2011.10.017" target="_blank">doi:</a><a title="" href="http://dx.doi.org/10.1038/nature11225" target="_blank">10.1016/j.cell.2011.10.017</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice</strong><br/>
Suzanne Devkota,1 Yunwei Wang,1 Mark W. Musch,1 Vanessa Leone,1 Hannah Fehlner-Peach,1 Anuradha Nadimpalli,1 Dionysios A. Antonopoulos,2 Bana Jabri1 & Eugene B. Chang1
The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health1. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2. This was associated with a pro-inflammatory T helper type 1 (TH1) immune response and increased incidence of colitis in genetically susceptible Il10?/?, but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10?/? mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
<br/>来源：生物谷
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