Giovannini C, Ciucci E, Cassetta M R, Cugini P, Facchinetti F
Department of Neuroendrocrinology, University of Rome, Italy.
Appetite. 1991 Feb;16(1):39-43. doi: 10.1016/0195-6663(91)90109-6.
Beta-endorphin (beta-Ep) plasma levels are higher in obese patients than in normal subjects. To establish that this finding constitutes hyperendorphinemia, 28 obese patients aged 12-55 years, six males and 22 females, (weighing 61-117 kg) were investigated twice by an overnight 1-mg p.o. dose dexamethasone suppression test (DST) before and after weight loss. beta-Ep was measured by radioimmunoassay (RIA). Before body weight loss, beta-Ep was higher than normal and unresponsive to DST, whereas ACTH and cortisol were suppressible. After weight loss, beta-Ep was slightly reduced but still insensitive to DST. ACTH and cortisol were responsive as usual. Findings suggest a resistance to DST in obesity as far as beta-Ep is concerned. The disorder persists even after weight loss, indicating that hyperendorphinemia is not secondary to body weight excess. Accordingly, one can argue that the unresponsiveness of the endorphinergic system to its physiological feedback is a pathophysiological characteristic of obesity.
肥胖患者血浆β-内啡肽（β-Ep）水平高于正常受试者。为确定这一发现是否构成高内啡肽血症，对28例年龄在12 - 55岁的肥胖患者（6名男性和22名女性，体重61 - 117千克）在减肥前后分别进行了两次口服1毫克地塞米松过夜抑制试验（DST）。采用放射免疫分析法（RIA）测定β-Ep。体重减轻前，β-Ep高于正常水平且对地塞米松抑制试验无反应，而促肾上腺皮质激素（ACTH）和皮质醇可被抑制。体重减轻后，β-Ep略有降低但对地塞米松抑制试验仍不敏感。ACTH和皮质醇则像往常一样有反应。研究结果表明，就β-Ep而言，肥胖患者对地塞米松抑制试验存在抵抗。即使体重减轻后这种紊乱仍然存在，这表明高内啡肽血症并非继发于体重过重。因此，可以认为内啡肽能系统对其生理反馈无反应是肥胖的一种病理生理特征。
