Serum insulin but not leptin is associated with spontaneous and growth hormone (GH)-releasing hormone-stimulated GH secretion in normal volunteers with and without weight loss.

Serum insulin but not leptin is associated with spontaneous and growth hormone (GH)-releasing hormone-stimulated GH secretion in normal volunteers with and without weight loss.
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在体重减轻或未减轻的正常志愿者中,血清胰岛素(而非瘦素)与自发的生长激素(GH)释放激素刺激的 GH 分泌相关。

DOI:
10.1016/s0026-0495(98)90288-8
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发表时间:
1998
期刊:
Metabolism: clinical and experimental
影响因子:
--
通讯作者:
Tayek,JA
Tayek,JA
中科院分区:
--
文献类型:
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作者:
Manglik,S;Cobanov,B;Flores,G;Nadjafi,R;Tayek,JA

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人类体重减轻与下丘脑-垂体生长激素(GH)分泌升高有关。本研究评估了体重减轻对14名正常体重(体重指数[BMI], 25±1 Kg/m2)受试者下丘脑-垂体(gh释放激素[GHRH]-GH)轴的影响,其中一半受试者经历了饮食引起的体重减轻14%±2%(平均值±SEM)。在体重维持1周后,测定两组的胰岛素样生长因子-1 (IGF-1)、胰岛素、口服葡萄糖耐量、瘦素和生长激素脉冲模式。值得注意的是,我们测试的是最近减肥(3个月)的效果,而不是最近的饮食摄入,因为在临床研究中心(CRC)的预研究中,两组人都摄入了正常卡路里的饮食2天。减肥组血清胰岛素(3.8±0.7 v 9.0±0.9 μU/mL, P < 0.01)、c肽(0.44±0.06 v 0.59±0.04 mg/mL, P < 0.05)显著降低。血清瘦素无明显差异。减肥组内源性GH脉冲高度(11.9±4.8 v 1.3±0.1 μg/L, P < 0.05)、每GH脉冲面积([AUC] 57±28 v 6±1 μg/L, P < 0.05)和平均GH(3.91±0.76 v 0.85±0.16 μg/L, P < 0.01)均升高。血清胰岛素水平与平均生长激素浓度呈负相关(r =−)。678, P < 0.01)和GH脉冲高度(r = - 7.33, P < 0.01)。除自发GH分泌外,减肥组ghrh刺激的GH脉冲高度(41.8±18.1 v 7.1±1.6 μg/L, P < 0.05)和AUC(161±35 v 46±13 μg/L/min, P < 0.05)也增加。胰岛素浓度也与ghrh刺激的GH脉冲高度呈负相关(r =−)。718, p < 0.01)。瘦素浓度与BMI (r = 0.554, P < 0.05)和体脂(r = 0.744, P < 0.01)相关,与GH分泌无关。综上所述,尽管这些患者的饮食热量正常,但在体重和健康正常的年轻男性和女性中,近期体重减轻的历史可能与自发生长激素脉冲高度和ghrh刺激脉冲高度的显着增加有关。体重减轻也与血清胰岛素水平降低有关。观察到的生长激素分泌的增加可能是继发于胰岛素的减少或作用于垂体部位的其他因素的改变。
Weight loss in humans is associated with elevated hypothalamic-pituitary growth hormone (GH) secretion. This study evaluates the effects of weight loss on the hypothalamic-pituitary (GH-releasing hormone [GHRH]-GH) axis in 14 normal-weight (body mass index [BMI], 25 ± 1 Kg/m2) subjects, of whom half had undergone a diet-induced weight loss of 14% ± 2% (mean ± SEM). Insulin-like growth factor-1 (IGF-1), insulin, oral glucose tolerance, leptin, and GH pulse patterns were determined in both groups after weight maintenance for 1 week. Of note, we tested the effects of recent weight loss (3 months) and not a recent dietary intake, since both groups ingested a normal calorie diet for 2 days in the Clinical Research Center (CRC) prestudy. Serum insulin (3.8 ± 0.7 v 9.0 ± 0.9 μU/mL, P < .01) and C-peptide (0.44 ± 0.06 v 0.59 ± 0.04 mg/mL, P < .05) were significantly lower in the weight loss group. Serum leptin was not different. Endogenous GH pulse height (11.9 ± 4.8 v 1.3 ± 0.1 μg/L, P < .05), area per GH pulse ([AUC] 57 ± 28 v 6 ± 1 μg/L, P < .05), and mean GH (3.91 ± 0.76 v 0.85 ± 0.16 μg/L, P < .01) were increased in the weight loss group. The serum insulin level was inversely associated with the mean GH concentration (r = −.678, P < .01) and GH pulse height (r = −7.33, P < .01). In addition to spontaneous GH secretion, the GHRH-stimulated GH pulse height (41.8 ± 18.1 v 7.1 ± 1.6 μg/L, P < .05) and AUC (161 ± 35 v 46 ± 13 μg/L/min, P < .05) were also increased in the weight loss group. The insulin concentration was also inversely correlated with the GHRH-stimulated GH pulse height (r = −.718, P < .01). The leptin concentration was correlated with the BMI (r = .554, P < .05) and body fat (r = .744, P < .01), but not with GH secretion. In summary, even though these patients were on a normal calorie diet, a history of recent weight loss in young men and women of normal weight and health can be associated with a significant increase in spontaneous GH pulse height and GHRH-stimulated pulse height. Weight loss was also associated with a reduced serum insulin level. The observed increase in GH secretion may be secondary to the reduction in insulin or alterations of other factors acting at the site of the pituitary.