Inter‐relationships of the chronobiotic, melatonin, with leptin and adiponectin: implications for obesity

Abstract

Obesity and its medical complications represent a significant problem throughout the world. In recent decades, mechanisms underlying the progression of obesity have been intensively examined. The involvement of both the behavioral aspects, such as calorie-rich diet, low physical activity and sleep deprivation, and the intrinsic factors, including adipose tissue deregulation, chronic inflammation, oxidative stress, and chronodisruption, has been identified. The circadian disturbances of the adipose tissue endocrine function have been correlated with obesity. Leptin and adiponectin are adipokines strongly associated with glucose and lipid metabolism and with energy balance. Their synthesis and secretion display circadian rhythms that are disturbed in the obese state. Hyperleptinemia resulting in leptin resistance, and hypo-adiponectinemia have been linked to the pathophysiology of the obesity-related disorders. A deficiency of melatonin, one of the consequences of sleep deprivation, has also been demonstrated to correlate with obesity. Melatonin is a pineal secretory product involved in numerous actions, such as regulation of internal biological clocks and energy metabolism, and it functions as an antioxidant and as an anti-inflammatory agent. There exists a substantial amount of evidence supporting the beneficial effects of melatonin supplementation on obesity and its complications. In the current review, the results of studies related to the interactions between melatonin, and both leptin and adiponectin are discussed. Despite the existence of some inconsistencies, melatonin has been found to normalize the expression and secretion patterns of both adipokines. These results support the concept of melatonin as a potential therapeutic agent for obesity and related disorders.

Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie-Restricted Diet

“…Both adiponectin and omentin-1 were found to improve insulin sensitivity [74, 76]. Increased levels of these adipokines after melatonin supplementation, observed in the present study, are consistent with the research of McMullan et al [95].…”

“…It improves insulin sensitivity, regulates appetite and energy expenditure, and exerts anti-inflammatory, antiproliferative, and antiapoptotic actions [76]. Adiponectin is produced in higher amounts in subcutaneous than in visceral WAT [77].…”

“…Moreover, it was demonstrated that adiponectin positively correlated with circadian amplitude of melatonin secretion in healthy women, but not in the metabolic syndrome women [84]. Many animal model studies confirmed the stimulatory effect of melatonin treatment on circulating adiponectin [31, 32, 85], but there exist some inconsistencies in other experiments [76]. Several mechanisms may participate in melatonin's influence on adiponectin secretion, including the impact of indoleamine on adiponectin signaling pathways, its antioxidant and anti-inflammatory properties, mitochondrial function improvement, and changes in other adipokine levels [23, 76, 86, 87].…”

Dietary Sources and Bioactivities of Melatonin

“…Obesity is also a strong risk factor for other metabolic diseases. Although obesity is a result of imbalance of energy intake and expenditure, many other factors are involved in and contribute to the obese conditions, such as chronic inflammation, oxidative stress, circadian disruption and sleep deprivation [281]. Melatonin has been reported to attenuate the damage caused by obesity.…”

Cardioprotective Effects of HuoxueAnshen Recipe against Myocardial Injuries Induced by Sleep Deprivation in Rats

“…It has been reported that endothelin (ET-1) and proinflammatory cytokines are significantly elevated after SD, while TNF-alpha (TNF- α ) is a primary mediator in triggering inflammation and apoptosis in myocardial injury [4, 5, 7]. In addition, deficiency of melatonin (MT) is one of the consequences of SD [8], while MT with anti-inflammatory and endothelium protective effects is involved in the modulation of cardiac dysfunction and myocardial ischemia/reperfusion (I/R) injury [9, 10]. Furthermore, SD is related to Bcl 2 and Bax expression, and nuclear transcription factor (NF- κ B) signaling system, which plays a pathogenic role in inflammation and myocardial apoptosis [5, 11].…”