Dataset Information

Effects of Inulin Propionate Ester on Obesity-Related Metabolic Syndrome and Intestinal Microbial Homeostasis in Diet-Induced Obese Mice.

ABSTRACT: 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.

SUBMITTER: Zhu X

PROVIDER: S-EPMC7288568 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Effects of Inulin Propionate Ester on Obesity-Related Metabolic Syndrome and Intestinal Microbial Homeostasis in Diet-Induced Obese Mice.

Zhu Xiaozhen X Zhang Xia X Gao Xuelu X Yi Yuetao Y Hou Yang Y Meng Xianyao X Jia Chenchen C Chao Bo B Fan Wenyong W Li Xinrui X Zhang Hanhan H

ACS omega 20200528 22

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 ...[more]

PMID: 32548470

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Project description:BackgroundC1q/tumor necrosis factor-related protein 1 (CTRP1) is an adipokine secreted by adipose tissue, related to chondrocyte proliferation, inflammation, and glucose homeostasis. However, the therapeutic effects on metabolic disorders and the underlying mechanism were unclear. Here, we investigated the functions and mechanisms of CTRP1 in treating obesity and diabetes.MethodsThe plasmid containing human CTRP1 was delivered to mice by hydrodynamic injection, which sustained expression of CTRP1 in the liver and high protein level in the blood. High-fat diet (HFD) fed mice and STZ-induced diabetes model were used to study the effects of CTRP1 on obesity, glucose homeostasis, insulin resistance, and hepatic lipid accumulation. The lipid accumulation in liver and adipose tissue, glucose tolerance, insulin sensitivity, food intake, and energy expenditure were detected by H&E staining, Oil-Red O staining, glucose tolerance test, insulin tolerance test, and metabolic cage, respectively. The metabolic-related genes and signal pathways were determined using qPCR and western blotting.ResultsWith high blood circulation, CTRP1 prevented obesity, hyperglycemia, insulin resistance, and fatty liver in HFD-fed mice. CTRP1 also improved glucose metabolism and insulin resistance in obese and STZ-induced diabetic mice. The metabolic cage study revealed that CTRP1 reduced food intake and enhanced energy expenditure. The mechanistic study demonstrated that CTRP1 upregulated the protein level of leptin in blood, thermogenic gene expression in brown adipose tissue, and the gene expression responsible for lipolysis and glycolysis in white adipose tissue (WAT). CTRP1 also downregulated the expression of inflammatory genes in WAT. Overexpression of CTRP1 activated AMPK and PI3K/Akt signaling pathways and inhibited ERK signaling pathway.ConclusionThese results demonstrate that CTRP1 could improve glucose homeostasis and prevent HFD-induced obesity and fatty liver through upregulating the energy expenditure and reducing food intake, suggesting CTRP1 may serve as a promising target for treating metabolic diseases.

Dataset Information

Effects of Inulin Propionate Ester on Obesity-Related Metabolic Syndrome and Intestinal Microbial Homeostasis in Diet-Induced Obese Mice.

Publications

Effects of Inulin Propionate Ester on Obesity-Related Metabolic Syndrome and Intestinal Microbial Homeostasis in Diet-Induced Obese Mice.

Similar Datasets

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