Utz A L, Yamamoto A, Sluss P, Breu J, Miller K K
Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
J Clin Endocrinol Metab. 2008 Oct;93(10):4033-40. doi: 10.1210/jc.2008-0930. Epub 2008 Jul 22.
Obesity is characterized by reduced GH secretion, but data regarding IGF-I levels and their determinants are conflicting.
The objectives were to determine whether IGF-I levels are reduced and to investigate determinants of GH and IGF-I in healthy overweight and obese women.
A cross-sectional study was performed.
The study was conducted at a General Clinical Research Center.
Thirty-four healthy women without pituitary/hypothalamic disease participated, including 11 lean [body mass index (BMI) <25 kg/m(2)], 12 overweight (BMI > or =25 kg/m(2) and <30 kg/m(2)), and 11 obese (BMI > or =30 kg/m(2)) women of comparable age (overall mean age, 30.7 +/- 7.8 yr).
There was no intervention.
The main outcome measures were frequent sampling (every 10 min for 24 h) for GH, peak GH after GHRH-arginine stimulation, IGF-I, IGF binding protein-3, estrone, estradiol, testosterone, free testosterone, SHBG, homeostasis model assessment of insulin resistance, and abdominal fat.
Mean 24-h GH and peak stimulated GH were lower in overweight than lean women and lowest in obese women. Mean IGF-I levels trended lower in obese, but not overweight, compared with lean women. Free testosterone was positively associated with IGF-I (R = 0.36, P = 0.04) but not with GH measures. Visceral fat was the only determinant of mean 24-h GH (R(2) = 0.66, P < 0.0001) and of peak stimulated GH (R(2) = 0.63, P < 0.0001), and mean 24-h GH accounted for 39% of the variability of IGF-I (P = 0.0002), with an additional 28% (P < 0.0001) attributable to free testosterone levels.
Despite a linear decrease in GH secretion and peak stimulated GH levels with increasing BMI in healthy overweight and obese women, IGF-I levels were not commensurately reduced. Androgens may contribute to this relative preservation of IGF-I secretion in overweight and obese women despite reduced GH secretion.
肥胖的特征是生长激素(GH)分泌减少,但关于胰岛素样生长因子-I(IGF-I)水平及其决定因素的数据存在矛盾。
确定IGF-I水平是否降低,并调查健康超重和肥胖女性中GH和IGF-I的决定因素。
进行了一项横断面研究。
研究在一个综合临床研究中心进行。
34名无垂体/下丘脑疾病的健康女性参与,包括11名瘦女性[体重指数(BMI)<25kg/m²]、12名超重女性(BMI≥25kg/m²且<30kg/m²)和11名肥胖女性(BMI≥30kg/m²),年龄相仿(总体平均年龄,30.7±7.8岁)。
无干预。
主要观察指标包括对GH进行频繁采样(每10分钟一次,共24小时)、生长激素释放激素-精氨酸刺激后的GH峰值、IGF-I、IGF结合蛋白-3、雌酮、雌二醇、睾酮、游离睾酮、性激素结合球蛋白、胰岛素抵抗的稳态模型评估以及腹部脂肪。
超重女性的平均24小时GH和刺激后GH峰值低于瘦女性,肥胖女性最低。与瘦女性相比,肥胖女性的平均IGF-I水平呈下降趋势,但超重女性并非如此。游离睾酮与IGF-I呈正相关(R = 0.36,P = 0.04),但与GH指标无关。内脏脂肪是平均24小时GH(R² = 0.66,P < 0.0001)和刺激后GH峰值(R² = 0.63,P < 0.0001)的唯一决定因素,平均24小时GH占IGF-I变异性的39%(P = 0.0002),另外28%(P < 0.0001)归因于游离睾酮水平。
尽管在健康超重和肥胖女性中,随着BMI增加GH分泌和刺激后GH峰值呈线性下降,但IGF-I水平并未相应降低。雄激素可能导致超重和肥胖女性尽管GH分泌减少,但IGF-I分泌仍相对保持。