Butyrate alleviates high fat diet-induced obesity through activation of adiponectin-mediated pathway and stimulation of mitochondrial function in the skeletal muscle of mice

• DOI: 10.18632/oncotarget.11267
• Publication Date: 2016-08-13T03:23:53Z
• Authors: Jian Hong; Yimin Jia; Shifeng Pan; Longfei Jia; Huifang Li; Zhenqiang Han; Demin Cai; Ruqian Zhao
• Keywords: UCP3; Sodium butyrate; AMP-Activated Protein Kinase; Adiponectin receptor 1

Dietary supplementation of butyrate can prevent diet-induced obesity through increasing mitochondrial function in mice, yet the up-stream signaling pathway remains elusive. In this study, weaned mice were divided into two groups, fed control (CON) and high-fat diet (HF, 45% energy from fat), respectively, for 8 weeks. HF-induced obese maintained on HF diet, then groups; HFB group was gavaged with 80 mg sodium (SB) per every other day 10 days, while received vehicle. It shown that five gavage doses SB significantly alleviated restored plasma glucose, insulin leptin to levels. Muscle contents ADP AMP increased, which associated enhanced oxidative phosphorylation up-regulated expression fatty acid oxidation enzymes uncoupling proteins, UCP2 UCP3 skeletal muscle. adiponectin receptors (adipoR1/2) kinase (AMPK), diminished histone deacetylase 1 (HDAC1). Higher H3K9Ac, a gene activation mark, detected promoter Adipor1/2, Ucp2 Ucp3 genes activated muscle SB-treated mice. Our results indicate short-term oral administration alleviate resistance adiponectin-mediated stimulation