创作:女巫 审核:mildbreeze 2018年10月30日
  • 给无菌小鼠定殖来自肥胖(Inf-ObMB)或正常体重(Inf-NWMB)母亲所生的2周龄婴儿的粪便菌群,并进行比较;
  • Inf-ObMB小鼠肝脏中内质网应激和先天免疫相关基因表达增加,并出现小儿非酒精性脂肪肝(NAFLD)中较常见的门静脉周围炎症的组织学特征;
  • Inf-ObMB小鼠的肠道通透性增加、巨噬细胞吞噬作用减弱、细胞因子产生减少,提示巨噬细胞功能受损;
  • Inf-ObMB小鼠暴露于西方饮食可促进体重过度增加并加速NAFLD发展。
Nature Communications近期上线的一项小鼠研究表明,来自胖妈所生的婴儿2周龄时的粪便菌群,可影响受体小鼠的代谢和炎症,促进小鼠肥胖和脂肪肝。这些发现证明,早期肠道菌群失调,在一定程度上介导了母体肥胖对后代肥胖和脂肪肝的促进作用。

The gut microbiota in infants of obese mothers increases inflammation and susceptibility to NAFLD



2018-10-26, Article

Abstract & Authors:展开

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.

First Authors:
Taylor K Soderborg

Correspondence Authors:
Jacob E Friedman

All Authors:
Taylor K Soderborg,Sarah E Clark,Christopher E Mulligan,Rachel C Janssen,Lyndsey Babcock,Diana Ir,Dominick J Lemas,Linda K Johnson,Tiffany Weir,Laurel L Lenz,Daniel N Frank,Teri L Hernandez,Kristine A Kuhn,Angelo D'Alessandro,Linda A Barbour,Karim C El Kasmi,Jacob E Friedman