Effects of fenofibrate on high-fat diet-induced body weight gain and adiposity in female C57BL/6J mice☆
Section snippets
Animal treatments
For all experiments, 8-week-old mice (C57BL/6J) were housed and bred at the Korea Research Institute of Bioscience and Biotechnology under pathogen-free conditions with a standard 12-hour light/dark cycle. Prior to the administration of special diets, mice were fed standard rodent chow and water ad libitum. Female Sham and OVX mice were each randomly divided into 3 groups (n = 5 per group), which showed the uniformity in response to each treatment in the pilot study. The mice received a low-fat
Effects of fenofibrate on body weight gain and WAT mass in female mice
To determine whether fenofibrate reduces body weight gain and adiposity in female mice, the influence of fenofibrate treatment on body weight and WAT mass was examined in diet-induced obese female Sham and OVX C57BL/6J mice. Compared to their respective low-fat diet controls, the administration of a high-fat diet for 13 weeks increased body weight by 15.7% ± 0.7% in OVX mice and by 8.4% ± 0.5% in Sham mice, as shown in Fig 1. In contrast, compared to their respective high-fat diet-fed groups,
Discussion
This study was undertaken to verify whether fenofibrate prevents body weight gain and adiposity in female OVX and Sham C57BL/6J mice on a high-fat diet, and to determine whether PPARα is associated with these events.
Our results demonstrate that fenofibrate reduces body weight gain and WAT mass in high-fat diet-fed OVX mice, but fails to do so in Sham mice. Body weights of OVX mice were found to be higher than those of Sham mice 6 weeks after commencing the high-fat diet. Compared to high-fat
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2018, Current Opinion in ToxicologyFish oil and fenofibrate inhibit pancreatic islet hypertrophy, and improve glucose and lipid metabolic dysfuntions with different ways in diabetic KK mice
2018, Obesity Research and Clinical PracticeCitation Excerpt :Fish oil activates PPARα and enhances the expression of genes involved in fatty acid oxidation and triglyceride hydrolysis such as acyl-CoA oxidase (AOX), lipoprotein lipase, medium-chain acyl-CoA dehydrogenase, acyl-CoA synthetase and uncoupling protein-2 (UCP-2) [16,17]. The clinical anti-hyperlipidemia drug fenofibrate, an agonist of PPARα, decreases triglyceride synthesis and increases hepatic fatty acid oxidation, reducing the amount of fatty acids available for triglyceride synthesis [18,19]. And, fenofibrate treatment lowers plasma concentration of triglycerides and low density lipoprotein (LDL) cholesterol, and raises the high density lipoprotein (HDL) cholesterol level [20,21].
Effect of Gangjihwan on hepatic steatosis and inflammation in high fat diet-fed mice
2017, Journal of EthnopharmacologyCitation Excerpt :The inhibitory effects of DF on obesity were comparable to those of the PPARα agonist fenofibrate. It was shown that PPARα activators reduced body weight gain and adipose tissue mass, at least in part, due to the increase of fatty acid oxidation (Jeong et al., 2004; Jeong and Yoon, 2009). Hypertrophied adipocytes secrete TNFα, leptin, free fatty acids, and high levels of inflammatory cytokines such as MCP-1, which are closely associated with metabolic syndromes including insulin resistance, type 2 diabetes, NAFLD, and cardiovascular disease (Xu et al., 2003; Curat et al., 2004; Despres and Lemieux, 2006; Jeong and Yoon, 2009).
Acyl CoA synthetase-1 links facilitated long chain fatty acid uptake to intracellular metabolic trafficking differently in hearts of male versus female mice
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Supported by a Grant No. KRF-2003-015-C00621 from Korea Research Foundation.