4.7 Article

Omija fruit ethanol extract improves adiposity and related metabolic disturbances in mice fed a high-fat diet

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 41, 期 -, 页码 137-141

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2016.12.016

关键词

Brown fat-selective genes; Fatty acid oxidation; Fecal lipid excretion; Insulin resistance; Omija fruit ethanol extract

资金

  1. Basic Science Research Program [NRF-2014R1A1A4A01007858, 2016R1D1A3B03931424]
  2. Science Research Center Project of the National Research Foundation of Korea - Ministry of Education, Science and Technology [NRF-2015R1A5A6001906]
  3. Pukyung National University Research Fund [C-D-2015-1253]

向作者/读者索取更多资源

This study investigated the biological and molecular mechanisms underlying the antiobesity effect of omija fruit ethanol extract (OFE) in mice fed a high-fat diet (HFD). C57BL/6J mice were fed an HFD (20% fat, w/w) with or without OFE (500 mg/kg body weight) for 16 weeks. Dietary OFE significantly increased brown adipose tissue weight and energy expenditure while concomitantly decreasing white adipose tissue (WAT) weight and adipocyte size by up-regulating the expression of brown fat-selective genes in WAT. OFE also improved hepatic steatosis and dyslipidemia by enhancing hepatic fatty acid oxidation-related enzymes activity and fecal lipid excretion. In addition to steatosis, OFE decreased the expression of pro-inflammatory genes in the liver. Moreover, OFE improved glucose tolerance and lowered plasma glucose, insulin and homeostasis model assessment of insulin resistance, which may be linked to decreases in the activity of hepatic gluconeogenic enzymes and the circulating level of gastric inhibitory polypeptide. These findings suggest that OFE may protect against diet-induced adiposity and related metabolic disturbances by controlling brown-like transformation of WAT, fatty acid oxidation, inflammation in the liver and fecal lipid excretion. Improved insulin resistance may be also associated with its antiobesity effects. (C) 2017 Elsevier Inc. All rights reserved.

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