期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-018-06929-0
关键词
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资金
- American Diabetes Association/Glaxo Smith Kline Targeted Research Award [1-13-GSK-13]
- NIH/NCATS Colorado Clinical and Translational Sciences Institute [TL1-TR001081]
- Children's Hospital Colorado Child Health Research Internship
- Webb-Waring early career grant
- NIH/National Institute of Allergy and Infectious Diseases [R01AI131662]
- University of Colorado GI and Liver Innate Immune Program
- NIH/National Institute of Diabetes and Digestive and Kidney Diseases [R01DK07864]
Maternal obesity is associated with increased risk for offspring obesity and non-alcoholic fatty liver disease (NAFLD), but the causal drivers of this association are unclear. Early colonization of the infant gut by microbes plays a critical role in establishing immunity and metabolic function. Here, we compare germ-free mice colonized with stool microbes (MB) from 2-week-old infants born to obese (Inf-ObMB) or normal-weight (Inf-NWMB) mothers. Inf-ObMB-colonized mice demonstrate increased hepatic gene expression for endoplasmic reticulum stress and innate immunity together with histological signs of periportal inflammation, a histological pattern more commonly reported in pediatric cases of NAFLD. Inf-ObMB mice show increased intestinal permeability, reduced macrophage phagocytosis, and dampened cytokine production suggestive of impaired macrophage function. Furthermore, exposure to a Western-style diet in Inf-ObMB mice promotes excess weight gain and accelerates NAFLD. Overall, these results provide functional evidence supporting a causative role of maternal obesity-associated infant dysbiosis in childhood obesity and NAFLD.
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