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Effects of Inulin Propionate Ester on Obesity-Related Metabolic Syndrome and Intestinal Microbial Homeostasis in Diet-Induced Obese Mice
Author(s) -
Xiaozhen Zhu,
Xia Zhang,
Xuelu Gao,
Yuetao Yi,
Yang Hou,
Xianyao Meng,
Chenchen Jia,
Bo H. Chao,
Wenyong Fan,
Xinrui Li,
Hanhan Zhang
Publication year - 2020
Publication title -
acs omega
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.779
H-Index - 40
ISSN - 2470-1343
DOI - 10.1021/acsomega.0c00649
Subject(s) - propionate , endocrinology , metabolic syndrome , medicine , glucose homeostasis , inulin , gut flora , peptide yy , insulin resistance , obesity , homeostasis , fatty liver , fatty acid , chemistry , biology , biochemistry , disease , receptor , neuropeptide y receptor , neuropeptide
Short-chain fatty acid (SCFA) plays an important role in improving obesity and related metabolic syndrome induced by high-fat diet. We used the prepared inulin propionate ester (IPE) as a system for the targeted release of propionate to the colon to elucidate the role of IPE in regulating obesity and metabolic syndrome, and intestinal microbial homeostasis, in diet-induced obese mice. With this strategy, IPE significantly increased the SCFA contents in the colon and resulted in significant body weight reduction, insulin resistance amelioration, and gastrointestinal hormone (glucagon-like peptide and peptide YY) secretion ( P < 0.05). The IPE intervention reduced liver fatty accumulation, which improved obesity-related fatty liver disease ( P < 0.05). IPE supplementation increased the richness and diversity of the microbial community and altered bacterial population at both the phylum and family level. Intestinal microbial results showed that the relative abundance of Desulfovibrionaceae and Erysipelotrichaceae, which promote the production of inflammatory factors, was reduced. Our results demonstrate that IPE can be used as an effective strategy for delivering propionate to obese mice colon, which can ameliorate obesity and associated metabolic syndrome and modify intestinal microbial homeostasis.

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