Obesity is defined as a condition of abnormal or excessive fat accumulation in white adipose tissue that results from the exacerbated consumption of calories associated with low energy expenditure. Fat accumulation in both adipose tissue and other organs contributes to a systemic inflammation leading to the development of metabolic disorders such as type 2 diabetes, hypertension, and dyslipidemia. Melatonin is a potent antioxidant and improves inflammatory processes and energy metabolism. Using male mice fed a high-fat diet (HFD—59% fat from lard and soybean oil; 9:1) as an obesity model, we investigated the effects of melatonin supplementation on the prevention of obesity-associated complications through an analysis of plasma biochemical profile, body and fat depots mass, adipocytes size and inflammatory cytokines expression in epididymal (EPI) adipose depot. Melatonin prevented a gain of body weight and fat depot mass as well as adipocyte hypertrophy. Melatonin also reversed the increase of total cholesterol, triglycerides and LDL-cholesterol. In addition, this neurohormone was effective in completely decreasing the inflammatory cytokines leptin and resistin in plasma. In the EPI depot, melatonin reversed the increase of leptin, Il-6, Mcp-1 and Tnf-α triggered by obesity. These data allow us to infer that melatonin presents an anti-obesity effect since it acts to prevent the progression of pro-inflammatory markers in the epididymal adipose tissue together with a reduction in adiposity.
The incidence of obese people worldwide is increasing every year and accumulating evidence indicates that dysregulated expression of adipokines, caused by excess adiposity and adipocyte dysfunction, has been linked to the pathogenesis of obesity‐linked complications. Melatonin, a hormone responsible for the synchronization of mammalian circadian rhythms, is related to beneficial effects on the control of obesity and its complications. In this work we evaluated the effects of melatonin supplementation on the production of adipokines in epididydimal (EPI) and inguinal (ING) fat depots from obese animals induced by a high‐fat‐diet (HFD). Male C57Bl/6j mice were divided into 3 groups: CO, animals fed with control diet; Obese, animals fed with HFD and Obese + melatonin, animals fed with HFD and supplemented with melatonin (1mg/kg). Melatonin presented a preventive effect on body weight gain and slowed down the effects on food and energy efficiency triggered by HFD. Adiponectin, IL‐6, leptin, and TNF‐α gene expression in ING and EPI fat depots were analysed. It was observed an increase (by 55 %, p <0.05) in adiponectin mRNA in ING depot when the animals received melatonin. There was an increase (3,7‐fold, p <0.05) in the IL‐6 mRNA expression in the EPI depot (but not in ING) in HFD group, that was prevented by melatonin supplementation. The same increase was observed on leptin expression in EPI adipose depot (6‐fold, p <0.05) from animals fed with HFD. Again, melatonin supplementation completely abolished this effect. Similarly, there was an increase (by 23‐fold, p <0.05) in the expression of this gene in the ING depot from HFD animals, and herein, we observed only a prevention trend (p = 0.0514) by melatonin on leptin mRNA in this fat depot. In both, EPI and ING depots, TNF‐α mRNA was significantly increased (by 5‐fold and 7‐fold respectively, p <0.05) in the HFD as compared to the CO group, but the melatonin supplementation not decreased this parameter. The protein analysis in these tissues (ING and EPI) performed by Elisa, showed that IL‐6 protein was increased (68%, p <0.05) in EPI fat depot from HFD group when compared to CO. This elevation was completely prevented when the animals were supplemented with melatonin. By the other side, no changes were observed between the groups concerning IL‐6 secretion in ING depot. The results obtained herein suggest that melatonin supplementation improves the adipokines expression in animais with obesity induced by a HFD, that is, it increases adiponectin while reducing the expression of inflammatory cytokines in adipose tissues. Together, these results show that melatonin supplementation had an protetive action on obesity complicationsSupport or Funding InformationFapesp (2015/03554‐2)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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