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苹果酸乳杆菌 APS1 与节食相结合通过调节小鼠肠道微生物组改善了肥胖治疗的效果。

A combination of Lactobacillus mali APS1 and dieting improved the efficacy of obesity treatment via manipulating gut microbiome in mice.

机构信息

Institute of Biotechnology, National Taiwan University, Taipei City, 106, Taiwan.

Agricultural Biotechnology Research Center, Academia Sinica, Taipei City, 115, Taiwan.

出版信息

Sci Rep. 2018 Apr 18;8(1):6153. doi: 10.1038/s41598-018-23844-y.

DOI:10.1038/s41598-018-23844-y
PMID:29670255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5906640/
Abstract

The difficulty of long-term management has produced a high rate of failure for obesity patients. Therefore, improving the efficacy of current obesity treatment is a significant goal. We hypothesized that combining a probiotic Lactobacillus mali APS1 intervention with dieting could improve the efficacy of obesity and hepatic steatosis treatment compared to dieting alone. Mice were fed a high-fat diet for 6 weeks and then treated with: saline + normal diet and APS1 + normal diet (NDAPS1) for 3 weeks. NDAPS1 accelerated body weight loss and reduced caloric intake and fat accumulation. The fecal microbiome showed that accelerating weight loss by NDAPS1 resulted in restoring intestinal microbiota toward a pre-obese state, with alteration of specific changes in the obesity-associated bacteria. APS1 manipulated the gut microbiome's obesity-associated metabolites, followed by regulation of lipid metabolism, enhancement of energy expenditure and inhibition of appetite. The specific hepatic metabolites induced by the APS1-manipulated gut microbiome also contributed to the amelioration of hepatic steatosis. Our results highlighted a possible microbiome and metabolome that contributed to accelerating weight loss following treatment with a combination of APS1 and dieting and suggested that probiotics could serve as a potential therapy for modulating physiological function and downstream of the microbiota.

摘要

长期管理的困难导致肥胖患者的失败率很高。因此,提高当前肥胖治疗的疗效是一个重要目标。我们假设,与单独节食相比,将益生菌马利乳杆菌 APS1 干预与节食相结合可以提高肥胖和肝脂肪变性治疗的疗效。将小鼠用高脂肪饮食喂养 6 周,然后用生理盐水+正常饮食和 APS1+正常饮食(NDAPS1)治疗 3 周。NDAPS1 加速体重减轻并减少热量摄入和脂肪堆积。粪便微生物组显示,NDAPS1 通过加速体重减轻导致肠道微生物群向肥胖前状态恢复,肥胖相关细菌发生特定变化。APS1 操纵肠道微生物群的肥胖相关代谢物,随后调节脂质代谢,增强能量消耗和抑制食欲。APS1 操纵的肠道微生物群引起的特定肝代谢物也有助于改善肝脂肪变性。我们的结果强调了一种可能的微生物组和代谢组,它们有助于加速 APS1 与节食相结合治疗后的体重减轻,并表明益生菌可能是调节微生物群及其下游生理功能的潜在治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/9c9e8439283b/41598_2018_23844_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/22b14ee1b237/41598_2018_23844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/5b41d0e45e0c/41598_2018_23844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/4f2cc058e8d0/41598_2018_23844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/972c325b7705/41598_2018_23844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/2493fcbc133c/41598_2018_23844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/3b046807c577/41598_2018_23844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/9c9e8439283b/41598_2018_23844_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/22b14ee1b237/41598_2018_23844_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/5b41d0e45e0c/41598_2018_23844_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/4f2cc058e8d0/41598_2018_23844_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/972c325b7705/41598_2018_23844_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/2493fcbc133c/41598_2018_23844_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/3b046807c577/41598_2018_23844_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c842/5906640/9c9e8439283b/41598_2018_23844_Fig7_HTML.jpg

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