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母体益生菌补充可通过改变大鼠的微生物和代谢组学特征来减少后代的脂肪肝发育。

Maternal prebiotic supplementation reduces fatty liver development in offspring through altered microbial and metabolomic profiles in rats.

机构信息

Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.

Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada.

出版信息

FASEB J. 2019 Apr;33(4):5153-5167. doi: 10.1096/fj.201801551R. Epub 2019 Jan 10.

DOI:10.1096/fj.201801551R
PMID:30629464
Abstract

A maternal high-fat/sucrose diet, in the presence of maternal obesity, can program increased susceptibility to obesity and metabolic disease in offspring. In particular, nonalcoholic fatty liver disease risk is associated with poor maternal nutrition and obesity status, which may manifest via alterations in gut microbiota. Here, we report that in a preclinical model of diet-induced maternal obesity, maternal supplementation of a high-fat/sucrose diet with the prebiotic oligofructose improves glucose tolerance, insulin sensitivity, and hepatic steatosis in offspring following a long-term high-fat/sucrose dietary challenge compared with offspring of untreated dams. These improvements are associated with alterations in gut microbial composition and serum inflammatory profiles in early life and improvements in inflammatory and fatty-acid gene expression profiles in tissues. Serum metabolomics analysis highlights potential metabolic links between the gut microbiota and the degree of steatosis, including alterations in 1-carbon metabolism. Overall, our data suggest that maternal prebiotic intake protects offspring against hepatic steatosis and insulin resistance following 21 wk of high fat/sucrose diet, which is in part due to alterations in gut microbiota.-Paul, H. A., Collins, K. H., Nicolucci, A. C., Urbanski, S. J., Hart, D. A., Vogel, H. J., Reimer, R. A. Maternal prebiotic supplementation reduces fatty liver development in offspring through altered microbial and metabolomic profiles in rats.

摘要

高脂肪/高蔗糖饮食会增加母体肥胖后代肥胖和代谢疾病的易感性。非酒精性脂肪肝疾病风险与母体营养和肥胖状况有关,这可能通过改变肠道微生物群来表现。在这里,我们报告了在饮食诱导的母体肥胖的临床前模型中,与未经处理的母体后代相比,用益生元低聚果糖补充高脂肪/高蔗糖饮食可改善长期高脂肪/高蔗糖饮食挑战后后代的葡萄糖耐量、胰岛素敏感性和肝脂肪变性。这些改善与早期肠道微生物组成和血清炎症特征的改变以及组织中炎症和脂肪酸基因表达谱的改善有关。血清代谢组学分析突出了肠道微生物群和脂肪变性程度之间的潜在代谢联系,包括 1 碳代谢的改变。总体而言,我们的数据表明,母体益生元摄入可保护后代免受 21 周高脂肪/高蔗糖饮食后的肝脂肪变性和胰岛素抵抗,这部分归因于肠道微生物群的改变。

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