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. Here, LEP is linked to hypertriglyceridemia.