期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 10, 页码 -出版社
MDPI
DOI: 10.3390/ijms21103434
关键词
microbiota; obesity; Type 2 diabetes; leptin; diet
资金
- National Institutes of Health [R01AG018915]
- Pepper Older Americans for Independence Center [P30AG21332]
- Department of Defense [W81XWH-18-1-0118, W81XWH-19-1-0236]
- Center for Diabetes, Obesity and Metabolism
- Wake Forest Baptist Medical Center
- National Center for Advancing Translational Sciences (NCATS), the National Institutes of Health [UL1TR001420]
The gut microbiome plays an important role in obesity and Type 2 diabetes (T2D); however, it remains unclear whether the gut microbiome could clarify the dietary versus genetic origin of these ailments. Moreover, studies examining the gut microbiome in diet- versus genetically induced obesity/T2D in the same experimental set-up are lacking. We herein characterized the gut microbiomes in three of the most widely used mouse models of obesity/T2D, i.e., genetically induced (leptin-deficient i.e., Lep(ob/ob); and leptin-receptor-deficient i.e., Lep(db/db)) and high-fat diet (HFD)-induced obese (DIO)/T2D mice, with reference to their normal chow-fed (NC) and low-fat-diet-fed (LF) control counterparts. In terms of beta -diversity, Lep(ob/ob) and Lep(db/db) mice showed similarity to NC mice, whereas DIO and LF mice appeared as distinct clusters. The phylum- and genus-level compositions were relatively similar in NC, Lep(ob/ob), and Lep(db/db) mice, whereas DIO and LF mice demonstrated distinct compositions. Further analyses revealed several unique bacterial taxa, metagenomic functional features, and their correlation patterns in these models. The data revealed that obesity/T2D driven by diet as opposed to genetics presents distinct gut microbiome signatures enriched with distinct functional capacities, and indicated that these signatures can distinguish diet- versus genetically induced obesity/T2D and, if extrapolated to humans, might offer translational potential in devising dietary and/or genetics-based therapies against these maladies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据