Various physiological factors such as an effect on adiponectin and leptin may have contributed to the overall effect of in vivo melatonin on glucose uptake, as previously discussed.10 In a preventative-treatment setting, 16 weeks of melatonin consumption, starting before the establishment of obesity, reduced hypertriglyceridaemia and increased high-density lipoprotein cholesterol levels in rats fed the same high-calorie diet.32 However, the exact mechanism whereby in vivo melatonin treatment affects glucose homeostasis and enhances insulin responsiveness is complex and not fully elucidated. This evidence concerns the gene LEP and Obesity.