Weaver J U, Kopelman P G, McLoughlin L, Forsling M L, Grossman A
Department of Metabolism and Endocrinology, Royal London Hospital, UK.
Clin Endocrinol (Oxf). 1993 Sep;39(3):345-50. doi: 10.1111/j.1365-2265.1993.tb02375.x.
The purpose of this study was to determine whether alterations in the hypothalamo-pituitary-adrenal axis and arginine vasopressin secretion, which have been associated with animal obesity, also occur in man.
Cross-sectional analysis of extremely obese women and normal weight controls.
Thirty-three obese premenopausal, non-diabetic women (mean age 31 years, mean body mass index (BMI) 41), and 15 normal weight controls (mean age 24 years, mean BMI 22).
Arginine vasopressin (AVP), ACTH, beta-lipotrophin and cortisol responses to insulin-induced hypoglycaemia (0.2 units Actrapid/kg body weight for obese; 0.15 unit/kg for controls) were measured. The obese women were further characterized by anthropometric measurements (weight, body mass index, fat distribution) and indices of insulin secretion/resistance: fasting insulin, insulin secretion during 75-g oral glucose tolerance test area under curve, insulin-stimulated glucose disposal and an index of insulin resistance. No significant differences were found in the basal levels of ACTH, AVP, beta-lipotrophin or cortisol. An augmented peak beta-LPH (n = 16, P < 0.02, the difference of the mean 3.65, 95% confidence interval 1.33-10) and ACTH (n = 16, P = 0.05, the difference of the mean 2.12, 95% CI 1.0-4.5) response were found in obese as compared with normal weight controls. Both ACTH and AVP areas under the curve were similar in both groups studied. There was additionally a direct positive association between the integrated ACTH response (area under the curve) and the weight of the obese subjects (P < 0.05, r2 = 0.265). The cortisol response was negatively correlated with insulin-stimulated glucose disposal (P < 0.01, r2 = 0.23), but not with other indices of insulin secretion/resistance (fasting insulin, oral glucose tolerance test area under the curve, index of insulin resistance) or fat distribution. Comparable responses to hypoglycaemia were seen for AVP and cortisol. There was no correlation between the ACTH, AVP or cortisol responses.
Obesity is associated with increased activity of the hypothalamo-pituitary-adrenal axis as supported by augmented ACTH and beta-lipotrophin secretion in response to insulin-induced hypoglycaemia and the positive association between the ACTH response and the body weight of obese women studied.
本研究旨在确定下丘脑 - 垂体 - 肾上腺轴的改变以及精氨酸加压素分泌（这些改变与动物肥胖相关）在人类中是否也会发生。
对极度肥胖女性和正常体重对照组进行横断面分析。
33名肥胖的绝经前非糖尿病女性（平均年龄31岁，平均体重指数（BMI）41），以及15名正常体重对照组（平均年龄24岁，平均BMI 22）。
测量了精氨酸加压素（AVP）、促肾上腺皮质激素（ACTH）、β - 促脂素和皮质醇对胰岛素诱导的低血糖（肥胖者为0.2单位Actrapid/kg体重；对照组为0.15单位/kg）的反应。通过人体测量（体重、体重指数、脂肪分布）以及胰岛素分泌/抵抗指标（空腹胰岛素、75克口服葡萄糖耐量试验曲线下面积的胰岛素分泌、胰岛素刺激的葡萄糖处置和胰岛素抵抗指数）对肥胖女性进行进一步特征描述。在ACTH、AVP、β - 促脂素或皮质醇的基础水平上未发现显著差异。与正常体重对照组相比，肥胖者的β - LPH峰值增加（n = 16，P < 0.02，平均差异3.65，95%置信区间1.33 - 10），ACTH峰值增加（n = 16，P = 0.05，平均差异2.12，95%CI 1.0 - 4.5）。在两组研究对象中，ACTH和AVP曲线下面积相似。此外，ACTH综合反应（曲线下面积）与肥胖受试者体重之间存在直接正相关（P < 0.05, r2 = 0.265）。皮质醇反应与胰岛素刺激的葡萄糖处置呈负相关（P < 0.01, r2 = 0.23），但与胰岛素分泌/抵抗的其他指标（空腹胰岛素、口服葡萄糖耐量试验曲线下面积、胰岛素抵抗指数）或脂肪分布无关。AVP和皮质醇对低血糖的反应相当。ACTH、AVP或皮质醇反应之间无相关性。
肥胖与下丘脑 - 垂体 - 肾上腺轴活性增加相关，这一结论得到了以下支持：对胰岛素诱导的低血糖，ACTH和β - 促脂素分泌增加，以及所研究的肥胖女性的ACTH反应与体重之间存在正相关。
