One year of insulin-like growth factor I treatment does not affect bone density, body composition, or psychological measures in postmenopausal women.
One year of insulin-like growth factor I treatment does not affect bone density, body composition, or psychological measures in postmenopausal women.
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DOI：
10.1210/jcem.86.4.7377
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发表时间：
2001-04
期刊：
影响因子：
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通讯作者：
A. Friedlander;G. Butterfield;S. Moynihan;Jeanine Grillo;M. Pollack;L. Holloway;L. Friedman;J. Yesavage;Dwight Matthias;Scott Lee;R. Marcus;A. Hoffman
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文献类型：
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作者：
A. Friedlander;G. Butterfield;S. Moynihan;Jeanine Grillo;M. Pollack;L. Holloway;L. Friedman;J. Yesavage;Dwight Matthias;Scott Lee;R. Marcus;A. Hoffman
随着年龄的增长，下丘脑-生长激素-胰岛素样生长因子-I轴的活性下降，一些衰老的分解代谢变化被归因于躯体更年期。这项研究的目的是确定IGF-I激素替代治疗1年对60岁以上健康、非肥胖、绝经后妇女的身体成分、骨密度和心理参数的影响。受试者(n=16，70.6+/-2.0岁，71.8+/-2.8 kg)被随机分配到自我注射IGF-I(每天两次，15微克/公斤)或安慰剂组，并在基线、6个月和1年的治疗时进行研究。在基线时，IGF-I组和安慰剂组之间的任何测量变量都没有显著差异。胰岛素样生长因子-I治疗组的空腹血胰岛素样生长因子-I水平在6个月(330.0+/-52.8)和12个月(297.7+/-40.8)显著高于基线水平(65.6+/-11.9 ng/m L)，但在安慰剂组没有变化。IGF-I治疗不影响循环中IGF结合蛋白-1和-3的水平。前臂、腰椎、髋部和全身的骨密度[由双能X射线吸收测量仪(DXA)测量]在两组中都没有改变。同样，在整个治疗干预过程中，DXA测量的瘦质量、脂肪质量或体脂百分比没有差异。尽管IGF-I受试者在12个月时餐后胰岛素水平较低，但IGF-I治疗并未改变肌肉力量值(握力、仰卧位、腿部按压)、血脂参数(胆固醇、高密度脂蛋白、低密度脂蛋白、甘油三酯)和餐后血糖处理的指标。IGF-I不影响骨转换标记物(骨钙素和I型胶原N-端肽)，但在基线、6个月和12个月时，服用雌激素的受试者的骨转换标记物显著低于不服用雌激素的受试者。最后，情绪和记忆的心理测量也没有因干预而改变。尽管最初打算招募更多的受试者，但在16名受试者完成方案后，这项研究停止了，因为上述初步分析表明，无论治疗方案如何，结果变量都没有发生变化。因此，我们得出结论，一年的IGF-I治疗剂量足以将循环IGF-I提高到年轻的正常值，并不是改变老年妇女的身体成分或血液参数或改善骨密度、力量、情绪或记忆力的有效手段。
The activity of the hypothalamic-GH-insulin-like growth factor I (hypothalamic-GH-IGF-I) axis declines with age, and some of the catabolic changes of aging have been attributed to the somatopause. The purpose of this investigation was to determine the impact of 1 yr of IGF-I hormone replacement therapy on body composition, bone density, and psychological parameters in healthy, nonobese, postmenopausal women over 60 yr of age. Subjects (n = 16, 70.6 +/- 2.0 yr, 71.8 +/- 2.8 kg) were randomly assigned to either the self-injection IGF-I (15 microg/kg twice daily) or placebo group and were studied at baseline, at 6 months, and at 1 yr of treatment. There were no significant differences between the IGF-I and placebo groups in any of the measured variables at baseline. Fasting blood IGF-I levels were significantly elevated above baseline values (65.6 +/- 11.9 ng/mL) at 6 months (330.0 +/- 52.8) and 12 months (297.7 +/- 40.8) in the IGF-I treated group but did not change in the placebo subjects. Circulating levels of IGF-binding protein-1 and -3 were unaffected by the IGF-I treatment. Bone mineral density of the forearm, lumbar spine, hip, and whole body [as measured by dual-energy x-ray absorptiometry (DXA)] did not change in either group. Similarly, there was no difference in DXA-measured lean mass, fat mass, or percent body fat throughout the treatment intervention. Muscle strength values (grip, bench press, leg press), blood lipid parameters (cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides), and measures of postmeal glucose disposal were not altered by IGF-I treatment, although postmeal insulin levels were lower in the IGF-I subjects at 12 months. IGF-I did not affect bone turnover markers (osteocalcin and type I collagen N-teleopeptide), but subjects who were taking estrogen had significantly lower turnover markers than subjects who were not on estrogen at baseline, 6 months, and 12 months. Finally, the psychological measures of mood and memory were also not altered by the intervention. Despite the initial intent to recruit additional subjects, the study was discontinued after 16 subjects completed the protocol, because the preliminary analyses above indicated that no changes were occurring in any outcome variables, regardless of treatment regimen. Therefore, we conclude that 1 yr of IGF-I treatment, at a dose sufficient to elevate circulating IGF-I to young normal values, is not an effective means to alter body composition or blood parameters nor improve bone density, strength, mood, or memory in older women.