Melatonin and metabolic regulation: a review

Abstract

Human life expectancy has increased over the past 50 years due to scientific and medical advances and higher food availability. However, overweight and obesity affect more than 50% of adults and 15% of infants and adolescents. There has also been a marked increase in the prevalence of metabolic syndrome in recent decades, which has been associated with a reduction in nocturnal pineal production of melatonin with aging and an increased risk of coronary diseases, type 2 diabetes mellitus (T2DM) and death. Melatonin is currently under intensive investigation in experimental animal models of diabetes, obesity and MS at pharmacological doses (between 5 and 20 mg kg(-1) body weight), demonstrating its capacity to ameliorate the total metabolic profile and its potential as an alternative to conventional drug therapies for the disorders associated with the MS, i.e. elevated systolic blood pressure, and impairment of glucose homeostasis, plasma lipid profile, inflammation, oxidative stress, and increased body weight. An especially significant finding is the induction by melatonin of white adipose tissue browning, which may be related to its effects against oxidative stress, uncoupling the mitochondrial bioenergetic process by enhancing the expression of uncoupled-protein-1 (UCP-1), which has been related to body weight reduction in experimental animals. Further research is required to improve knowledge of this mechanism. Clinical studies are needed with the administration of pharmacological melatonin doses, because the dose has ranged between 0.050 and 0.16 mg kg(-1) bw in most studies to date. Melatonin is a natural phytochemical, and it is also important to test its beneficial metabolic effects when consumed in functional foods.

Melatonin as an antioxidant: under promises but over delivers

“…There should be long duration trials of melatonin against serious diseases (where few treatments are available) where it has been shown beneficial in limited clinical studies or where the experimental evidence is compelling. Some examples include melatonin's ability to forestall Alzheimer's disease, Parkinson's disease, multiple sclerosis, osteoporosis, diabetes and metabolic syndrome, sepsis, cancer, tropical diseases, snake and nematocyst venom toxicity, etc. In some cases, rather than a treatment for these conditions, melatonin should be more strongly considered in terms of its preventative actions as prevention always trumps treatment and is usually less expensive and certainly less debilitating.…”

Melatonin increases intracellular calcium in the liver, muscle, white adipose tissues and pancreas of diabetic obese rats

“…[1][2][3][4][5] The widespread presence of melatonin and its variety of biological properties suggest that it is a very ancient molecule with important roles in phylogenetic distant organisms. 2,[7][8][9] Melatonin has been found to exert an antioxidant effect via different mechanisms, 7,8,[10][11][12] confirming its role in the control of inflammation and oxidative stress, which underlie various chronic diseases. 2,[7][8][9] Melatonin has been found to exert an antioxidant effect via different mechanisms, 7,8,[10][11][12] confirming its role in the control of inflammation and oxidative stress, which underlie various chronic diseases.…”

The effects of antibiotics and melatonin on hepato-intestinal inflammation and gut microbial dysbiosis induced by a short-term high-fat diet consumption in rats

“…As the major regulator of circadian rhythm and an antioxidant hormone, melatonin adjusts the energy balance by reducing adipose tissue and improves diseases related to abnormal fat metabolism (35) . Long-term treatment with melatonin reduced body weight and intra-abdominal adiposity and prevented metabolic abnormalities induced by high-energy diet or ageing (36,37) .…”