Our cohort, showed the classical features of obesity and type 2 diabetes and, interestingly, lower GNE-9605 levels of cortisol and melatonin. Both hormones are usually studied as a measurement of the circadian state due to their different peaks throughout the day. Higher levels of cortisol have been related to obesity and central obesity conditions such as Cushing syndrome, however some studies have reported an inverse correlation between BMI and cortisol levels, similar to what we observed in our population. A higher clearance of cortisol due to obesity as well as a deregulation of the circadian secretion of cortisol with higher levels at night and lower levels in the morning are possible explanations for our findings. Likewise, melatonin has been found in higher levels in lean subjects. Melatonin is synthesized in the pineal gland and not only regulates the circadian and seasonal rhythms but also has antioxidant effects and is implicated in the control of glucose and lipid metabolism. Previous studies showed higher levels of nocturnal melatonin in obese than in BMI-matched type 2 diabetes and lean groups, without any differences among groups at other moments during the day. Moreover, melatonin is negatively correlated with features of metabolic syndrome in obese women, indicating that changes not only in the amplitude but also in the circadian secretion of melatonin could be associated with alterations in metabolism found in obesity and insulin resistance. Although a single point measure is not indicative of the complete daily secretion of both cortisol and melatonin, our results nevertheless support previous work relating obesity and type 2 diabetes with chronodisruption. On another note, we found that the AA-carriers C7280948 including all obese subjects exhibited a 2.46 fold-risk of developing obesity as compared to the AG-carriers and a 2.28 fold-risk as compared to the GG-carriers. Moreover, the AA-carriers exhibited a higher BMI and waist circumference than their non-carriers counterparts, demonstrating that the presence of the AA genotype is correlated with clinical traits of obesity.