LAUSR

OBJECTIVE Hypercortisolism is a risk factor for obesity. Cortisol increases in response to food intake in lean subjects. In obese subjects, disturbances of the food-induced cortisol peak were reported, but data from sufficiently powered and well-controlled trials are lacking. Understanding the cortisol response to food is essential as amplified, or recurrent cortisol surges could lead to hypercortisolism and contribute to obesity. Therefore, we investigate the cortisol response to food in lean and obese subjects. DESIGN This is a non-randomized, open-label study. METHODS We assessed serum cortisol values after a high-calorie meal in lean and obese male subjects. Cortisol levels were frequently assessed before and for 3 hours after food intake. RESULTS 36 subjects (18 lean, 18 obese) were included. There was no difference in overall cortisol levels between both groups during the study (area under the curve (AUC) obese: 55409 ±16994, lean: 60334 ±18001, p=0.4). Total cortisol levels reached peak concentrations 20 minutes after food intake in both groups; the maximum cortisol increase was similar in both groups (cortisol increase obese: 69.6 ±135.5 nmol/l, lean: 134.7 ±99.7 nmol/l; p=0.1). There was no correlation between body mass index (BMI) and baseline cortisol values (R2=0.001, p=0.83), cortisol increase (R2= 0.05, p=0.17), or cortisol AUC (R2= 0.03, p=0.28). CONCLUSIONS This study demonstrates that high-calorie food intake causes an immediate and substantial cortisol response in lean and obese subjects and is independent of body weight.