Abstract
Obesity results from critical periods of positive energy balance characterized by caloric intake greater than energy expenditure. This disbalance promotes adipose tissue dysfunction which is related to other comorbidities. Melatonin is a low-cost therapeutic agent and studies indicate that its use may improve obesity-related disorders. To evaluate if the melatonin is efficient in delaying or even blocking the damages caused by excessive ingestion of a high-fat diet (HFD) in mice, as well as improving the inflammatory profile triggered by obesity herein, male C57BL/6 mice of 8 weeks were induced to obesity by a HFD and treated for 10 weeks with melatonin. The results demonstrate that melatonin supplementation attenuated serum triglyceride levels and total and LDL cholesterol and prevented body mass gain through a decreased lipogenesis rate and increased lipolytic capacity in white adipocytes, with a concomitant increment in oxygen consumption and Pgc1a and Prdm16 expression. Altogether, these effects prevented adipocyte hypertrophy caused by HFD and reflected in decreased adiposity. Finally, melatonin supplementation reduced the crown-like-structure (CLS) formation, characteristic of the inflammatory process by macrophage infiltration into white adipose tissue of obese subjects, as well as decreased the gene expression of inflammation-related factors, such as leptin and MCP1. Thus, the melatonin can be considered a potential therapeutic agent to attenuate the metabolic and inflammatory disorders triggered by obesity.
Highlights
Obesity is a worldwide problem and represents a serious public health challenge for the 21’st century
Considering that obesity leads to a dysfunction of the main metabolic processes of white adipose tissue (WAT), the present study aims to evaluate if the melatonin is efficient in attenuating or even blocking the damages in WAT caused by the ingestion of a high-fat diet (HFD), as well as improving the inflammatory condition triggered by the HFDinduced obesity in mice
The Obese+Mel group presented a significant increment on body weight when compared to control (low fat) diet (Control) only from week 4 and completed the experimental protocol with the body mass ∼28% higher (p < 0.05) than Control group, but 13% lower (p < 0.05) than Obese group (Figure 1A), both groups presented the same pattern of food and fat ingestion (Figure 1B)
Summary
Obesity is a worldwide problem and represents a serious public health challenge for the 21’st century. It is known that adipocyte hypertrophy leads to morbid obesity [2, 3] characterized by the rapid growth of the fat depots through enlargement of existing fat cells, which is accompanied by a high degree of M1 macrophage infiltration, limited vessel development, and massive fibrosis [3]. Considering these facts, such pathological expansion is associated with chronic inflammation and a WAT dysfunction
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