State Key Laboratory of Microbial Metabolism, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
ISME J. 2012 Oct;6(10):1848-57. doi: 10.1038/ismej.2012.27. Epub 2012 Apr 12.
Disruption of the gut microbiota by high-fat diet (HFD) has been implicated in the development of obesity. It remains to be elucidated whether the HFD-induced shifts occur at the phylum level or whether they can be attributed to specific phylotypes; additionally, it is unclear to what extent the changes are reversible under normal chow (NC) feeding. One group (diet-induced obesity, DIO) of adult C57BL/6J mice was fed a HFD for 12 weeks until significant obesity and insulin resistance were observed, and then these mice were switched to NC feeding for 10 weeks. Upon switching to NC feeding, the metabolic deteriorations observed during HFD consumption were significantly alleviated. The second group (control, CHO) remained healthy under continuous NC feeding. UniFrac analysis of bar-coded pyrosequencing data showed continued structural segregation of DIO from CHO on HFD. At 4 weeks after switching back to NC, the gut microbiota in the DIO group had already moved back to the CHO space, and continued to progress along the same age trajectory and completely converged with CHO after 10 weeks. Redundancy analysis identified 77 key phylotypes responding to the dietary perturbations. HFD-induced shifts of these phylotypes all reverted to CHO levels over time. Some of these phylotypes exhibited robust age-related changes despite the dramatic abundance variations in response to dietary alternations. These findings suggest that HFD-induced structural changes of the gut microbiota can be attributed to reversible elevation or diminution of specific phylotypes, indicating the significant structural resilience of the gut microbiota of adult mice to dietary perturbations.
高脂肪饮食（HFD）引起的肠道微生物群落紊乱与肥胖的发生有关。目前尚不清楚这种 HFD 诱导的转变是发生在门水平还是可以归因于特定的生物型；此外，在正常饮食（NC）喂养下，这些变化在多大程度上是可逆的还不清楚。一组成年 C57BL/6J 小鼠（饮食诱导肥胖，DIO）接受 HFD 喂养 12 周，直到出现明显肥胖和胰岛素抵抗，然后这些小鼠切换到 NC 喂养 10 周。在切换到 NC 喂养后，HFD 消耗期间观察到的代谢恶化明显缓解。第二组（对照，CHO）在连续 NC 喂养下保持健康。对条形码焦磷酸测序数据的 UniFrac 分析表明，DIO 继续与 CHO 在 HFD 上分离。在切换回 NC 后的 4 周，DIO 组的肠道微生物群已经回到 CHO 空间，并沿着相同的年龄轨迹继续前进，在 10 周后完全与 CHO 融合。冗余分析确定了 77 个对饮食干扰有反应的关键生物型。随着时间的推移，这些生物型的 HFD 诱导变化都恢复到 CHO 水平。尽管这些生物型的丰度因饮食变化而显著变化，但其中一些生物型表现出强烈的与年龄相关的变化。这些发现表明，HFD 诱导的肠道微生物群落结构变化可以归因于特定生物型的可逆增加或减少，表明成年小鼠肠道微生物群落对饮食干扰具有显著的结构弹性。
