Korbonits M, Trainer P J, Nelson M L, Howse I, Kopelman P G, Besser G M, Grossman A B, Svec F
Department of Endorinology, St Bartholomew's Hospital, London, UK.
Clin Endocrinol (Oxf). 1996 Dec;45(6):699-706. doi: 10.1046/j.1365-2265.1996.8550865.x.
It has been previously shown that food intake elevates circulating ACTH and cortisol levels, but no report has been published regarding the changes in circulating dehydroepiandrosterone (DHEA). DHEA was originally described as a weak androgen, but more recently it has been associated with a wide range of metabolic functions. In addition, previous studies have described a hyper-responsive hypothalamo-pituitary-adrenal axis in obese subjects in response to various stimuli, but the specific response to food has not been studied.
We studied the effect of food on the hypothalamo-pituitary-adrenal axis in 20 subjects of normal body mass index (BMI range 18-25) and also in a group of 12 obese subjects (BMI range 34-61). Levels of glucose, insulin, ACTH, cortisol and dehydroepiandrosterone were measured every 20 minutes.
A small rise in DHEA accompanies the rise in circulating ACTH and cortisol in response to food in both lean and obese subjects, but DHEA rose independently of cortisol and ACTH on the fasting day. In the obese subjects, food induced a significantly greater change in serum cortisol (peak cortisol rise (mean +/- SEM); normal-weight group, 169 +/- 14%; obese group, 294 +/- 23%) and in the cortisol/DHEA ratio (area under the curve; normal-weight group, 202 +/- 15%; obese group, 292 +/- 29%) than in the normal-weight subjects. This difference was particularly notable in those with central-type obesity (waist/hip ratio > 0.80). A group of the normal, jean female subjects showed no cortisol rise after food intake.
Our results suggest that DHEA may vary independently of circulating cortisol, and that the cortisol response to food is enhanced in obese subjects, particularly in those with central obesity. We speculate that there may be a caused connection between the cortisol response to food in normal subjects, and the subsequent distribution of fat if such subjects overeat sufficiently to become obese.
先前的研究表明食物摄入会使循环中的促肾上腺皮质激素（ACTH）和皮质醇水平升高，但关于循环中的脱氢表雄酮（DHEA）变化尚无相关报道。DHEA最初被描述为一种弱雄激素，但最近发现它与多种代谢功能有关。此外，先前的研究描述了肥胖受试者的下丘脑-垂体-肾上腺轴对各种刺激反应过度，但对食物的具体反应尚未进行研究。
我们研究了食物对20名体重指数正常（BMI范围为18 - 25）的受试者以及12名肥胖受试者（BMI范围为34 - 61）下丘脑-垂体-肾上腺轴的影响。每20分钟测量一次血糖、胰岛素、ACTH、皮质醇和脱氢表雄酮的水平。
在瘦人和肥胖受试者中，食物摄入导致循环中的ACTH和皮质醇升高时，DHEA会有小幅升高，但在禁食日DHEA的升高独立于皮质醇和ACTH。在肥胖受试者中，食物引起的血清皮质醇变化（皮质醇峰值升高（平均值±标准误）；正常体重组，169±14%；肥胖组，294±23%）以及皮质醇/脱氢表雄酮比值变化（曲线下面积；正常体重组，202±15%；肥胖组，292±29%）比正常体重受试者更为显著。这种差异在中心型肥胖（腰臀比>0.80）者中尤为明显。一组正常体重的年轻女性受试者在进食后皮质醇未升高。
我们的结果表明DHEA可能独立于循环中的皮质醇而变化，并且肥胖受试者对食物的皮质醇反应增强，尤其是中心型肥胖者。我们推测正常受试者对食物的皮质醇反应与随后脂肪分布之间可能存在因果联系，如果这些受试者过度进食而变得肥胖的话。
