Abstract
Introduction: There are more than 2.2 billion overweight and obese people worldwide. Sleep imbalance and the resulting reduction in melatonin (MEL) concentrations in the human body have a significant impact on health, particularly the development of obesity and comorbidities. Objective: This was to conduct a systematic review of the main approaches and clinical studies on melatonin regulation in the control and treatment of obesity and its comorbidities. Methods: The PRISMA rules for systematic review were followed. This study included review articles, systematic reviews/meta-analyses, prospective studies, retrospective studies, and randomized, double-blind, placebo-controlled trials in humans. Results and Conclusion: 27 of the 30 studies were selected to compose the results of this systematic review. Most studies presented homogeneity in their results, with X2=83.3%>50%. It was concluded that melatonin is an important participant in the regulation of energy metabolism, including body weight, insulin sensitivity, and glucose tolerance. Randomized placebo-controlled clinical studies have shown that daily melatonin consumption can be effective in controlling blood pressure, including systemic blood pressure, mean arterial pressure and pulse pressure, and reduces anthropometric indices of obesity in patients, as it increases the mass and activity of brown adipose tissue, functioning as an anti-obesogenic hormone. Melatonin can regulate adipose tissue and adipokines, such as adipocyte lipolysis and fat deposition. Furthermore, melatonin can interact with intracellular molecules, acting as an effective antioxidant. Several studies have indicated a higher risk of developing obesity in people who sleep less than six hours a day. Hormonal changes that occur during sleep deprivation may explain the increase in caloric intake and decrease in leptin, increase in ghrelin and peptide YY. Melatonin also regulates food intake by controlling the production and secretion of insulin, glucagon, and cortisol. Epidemiological studies have shown a link between sleep deprivation, insulin resistance, and T2DM.