Albala C, Yáñez M, Devoto E, Sostin C, Zeballos L, Santos J L
Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
Int J Obes Relat Metab Disord. 1996 Nov;20(11):1027-32.
Obesity is considered a protective factor for osteoporosis improving bone mass and maintaining higher levels of estrogen during menopause.
To determine the association of obesity with bone mineral density (BMD), and its relationship with sex hormone levels.
A case-control study in Caucasian obese and non obese postmenopausal women.
113 obese and 50 non-obese postmenopausal women.
BMD (dual-photon X-ray absorptiometry) at cervical femur. Ward's triangle, proximal radius and lumbar spine. Plasma levels of glucose, insulin, total estrogen, follicle stimulating hormone (FSH), sex hormone binding globulin (SHBG), dehydroepiandrosterone sulfate (DHA-S) and testosterone.
Mean BMD at femoral sites were significantly higher in obese women (femoral neck: 0.849 +/- 0.124 g/cm2 vs 0.753 +/- 0.095 g/cm2, P < 0.001; Ward's triangle: 0.634 +/- 0.134 g/cm2 vs. 0.553 +/- 0.100 g/cm2, P < 0.001). Mean BMD at lumbar spine was 0.906 +/- 0.138 g/cm2 in obese women and 0.849 +/- 0.137 g/cm2 in non obese, P < 0.017. A decreased risk of osteopenia in femoral neck (Age adjusted OR = 0.36, 95%CI 0.17-0.75) and in lumbar spine (Age adjusted OR = 0.43, 95%CI 0.20-0.91) in obese women was observed. Although total estrogen were similar in both groups, in obese women, SHBG was lower (68.6 +/- 26.84 nmol/l vs. 85.1 +/- 31.18 nmol/l, P < 0.001), and postglucose load insulin levels were higher, than in non obese (77.2 +/- 50.4 Ul/ml vs. 49.4 +/- 24.1 Ul/ml, P < 0.0005).
The findings confirm a higher BMD in obese women and suggest that obesity exerts protection due to a decreased SHBG thus increasing free sex steroids. Besides, hyperinsulinemia may produce a decline in the production of IGFBG-1, leading to an increase of IGF-1, that may stimulate the proliferation of osteoblasts.
肥胖被认为是骨质疏松症的一个保护因素，可改善骨量并在绝经期间维持较高水平的雌激素。
确定肥胖与骨密度（BMD）的关联及其与性激素水平的关系。
一项针对白人肥胖和非肥胖绝经后女性的病例对照研究。
113名肥胖绝经后女性和50名非肥胖绝经后女性。
股骨颈、沃德三角区、桡骨近端和腰椎的骨密度（双能X线吸收法）。血浆葡萄糖、胰岛素、总雌激素、促卵泡激素（FSH）、性激素结合球蛋白（SHBG）、硫酸脱氢表雄酮（DHA-S）和睾酮水平。
肥胖女性股骨部位的平均骨密度显著更高（股骨颈：0.849±0.124g/cm² 对比 0.753±0.095g/cm²，P<0.001；沃德三角区：0.634±0.134g/cm² 对比 0.553±0.100g/cm²，P<0.001）。肥胖女性腰椎的平均骨密度为0.906±0.138g/cm²，非肥胖女性为0.849±0.137g/cm²，P<0.017。观察到肥胖女性股骨颈（年龄调整OR=0.36，95%CI 0.17 - 0.75）和腰椎（年龄调整OR=0.43，95%CI 0.20 - 0.91）发生骨质减少的风险降低。尽管两组的总雌激素水平相似，但肥胖女性的SHBG较低（68.6±26.84nmol/l对比85.1±31.18nmol/l，P<0.001），且葡萄糖负荷后胰岛素水平高于非肥胖女性（77.2±50.4Ul/ml对比49.4±24.1Ul/ml，P<0.0005）。
研究结果证实肥胖女性的骨密度较高，并表明肥胖通过降低SHBG从而增加游离性类固醇发挥保护作用。此外，高胰岛素血症可能导致IGFBG - 1生成减少，从而使IGF - 1增加，这可能刺激成骨细胞增殖。
