Holte J, Bergh T, Berne C, Wide L, Lithell H
Department of Obstetrics and Gynecology, Uppsala University, Sweden.
J Clin Endocrinol Metab. 1995 Sep;80(9):2586-93. doi: 10.1210/jcem.80.9.7673399.
The impact of weight reduction on metabolic, endocrine, and anthropometric variables was studied in 13 obese, insulin-resistant women with the polycystic ovary syndrome (PCOS). Insulin sensitivity (euglycemic insulin clamp), insulin secretion and glucose tolerance (iv glucose tolerance test), basal sex steroid hormones, gonadotropins and free fatty acids (FFA), skin folds and waist hip ratio (WHR) were evaluated before (PCO-BD) and after (PCO-AD) diet-induced weight reduction to a weight stable level [mean (SD) diet duration 14.9 (6.2) months]. Mean weight loss was 12.4 kg (4.7; P < 0.0001), equalling a reduction from a body mass index (BMI) of 32.2 (3.7) kg/m2 to 27.6 (3.7; P < 0.0001) kg/m2. The results were compared with those of two groups of weight stable (no diet) women, 21 with PCOS (PCO-ND) and 23 normal control subjects (C), who were matched to the BMI the diet group reached after weight loss. Insulin sensitivity index (M/I) improved on average 132% (P < 0.001) and plasma FFA by 32% (P < 0.01), serum sex hormone binding globulin levels increased by 35% (P < 0.01), and the sum of truncal-abdominal skin-folds (subscapular, umbilical, and suprailiacal) were reduced by 28% (P < 0.0001), whereas the early insulin response to iv glucose, the levels of gonadotropins and androstenedione, and the femoral sc fat did not change significantly with weight loss. M/I, levels of SHBG and FFA and truncal-abdominal fat reached levels similar to the controls, whereas PCO-ND had lower M/I (P < 0.01) and SHBG levels (P < 0.0001), greater concentrations of FFA (P < 0.01) and truncal-abdominal fat (P < 0.05) than C. Among women with normal glucose tolerance, the insulin increment was higher in both PCO-AD (P < 0.05) and PCO-ND (P < 0.01) than in C. There was a strong correlation between M/I and sum of truncal-abdominal skinfolds in all groups (PCO-BD: r = 0.82; P < 0.001, PCO-AD: r = 0.68; P < 0.05, PCO-ND: r = 0.81; P < 0.0001, C: r = 0.44; P < 0.05). The variation in M/I in PCO-AD and PCO-ND (pooled) was best explained by FFA and truncal-adbominal fat (model R2 = 0.67). In conclusion, insulin resistance in obese women with PCOS was reduced by weight loss to similar levels as BMI-matched control subjects, suggesting that insulin resistance in PCOS is not a feature of PCOS per se.(ABSTRACT TRUNCATED AT 400 WORDS)
对13名患有多囊卵巢综合征（PCOS）的肥胖、胰岛素抵抗女性进行了体重减轻对代谢、内分泌和人体测量学变量影响的研究。在饮食诱导体重减轻至体重稳定水平之前（PCO - BD）和之后（PCO - AD）[平均（标准差）饮食持续时间14.9（6.2）个月]，评估胰岛素敏感性（正常血糖胰岛素钳夹法）、胰岛素分泌和葡萄糖耐量（静脉葡萄糖耐量试验）、基础性激素、促性腺激素和游离脂肪酸（FFA）、皮褶厚度和腰臀比（WHR）。平均体重减轻12.4 kg（4.7；P < 0.0001），相当于体重指数（BMI）从32.2（3.7）kg/m²降至27.6（3.7；P < 0.0001）kg/m²。将结果与两组体重稳定（未节食）的女性进行比较，21名患有PCOS（PCO - ND）和23名正常对照受试者（C），他们与节食组体重减轻后达到的BMI相匹配。胰岛素敏感性指数（M/I）平均提高132%（P < 0.001），血浆FFA降低32%（P < 0.01），血清性激素结合球蛋白水平升高35%（P < 0.01），躯干 - 腹部皮褶厚度总和（肩胛下、脐部和髂嵴上）减少28%（P < 0.0001），而静脉注射葡萄糖后的早期胰岛素反应、促性腺激素和雄烯二酮水平以及股部皮下脂肪随体重减轻无显著变化。PCO - AD组的M/I、SHBG和FFA水平以及躯干 - 腹部脂肪达到与对照组相似的水平，而PCO - ND组的M/I（P < 0.01）和SHBG水平（P < 0.0001）低于C组，FFA（P < 0.01）和躯干 - 腹部脂肪（P < 0.05）浓度高于C组。在糖耐量正常的女性中，PCO - AD组（P < 0.05）和PCO - ND组（P < 0.01）的胰岛素增量均高于C组。所有组中M/I与躯干 - 腹部皮褶厚度总和之间均存在强相关性（PCO - BD：r = 0.82；P < 0.001，PCO - AD：r = 0.68；P < 0.05，PCO - ND：r = 0.81；P < 0.0001，C：r = 0.44；P < 0.05）。FFA和躯干 - 腹部脂肪最能解释PCO - AD组和PCO - ND组（合并）M/I的变化（模型R² = 0.67）。总之，肥胖的PCOS女性通过体重减轻，胰岛素抵抗降低至与BMI匹配的对照受试者相似的水平，这表明PCOS中的胰岛素抵抗本身并非PCOS的特征。（摘要截断于400字）
