Milewicz A, Demissie M, Zatonska K, Jedrzejuk D, Tworowska U, Ilow R, Biernat J
Department of Endocrinology and Diabetology, Wrocław Medical University, Wybrzeze L. Pasteura 4, 50-367 Wrocław, Poland.
Gynecol Endocrinol. 2003 Aug;17(4):333-8.
This preliminary study addressed the possible associations between dietary, genetic and hormonal factors that are involved in the development of menopausal obesity and its metabolic consequences. We performed anthropometrical, hormonal and biochemical measurements and used a nutritional questionnaire on 43 postmenopausal women who were non-HRT-users (14 obese and 29 non-obese subjects, mean age +/- SD of 52.8 +/- 4.6 years, mean body mass 74.6 +/- 4.6 kg). All of the women also had fat mass assessed by DPX-Lunar. From the 24-h dietary recall, the nutrient intake in daily food rations was calculated using a computer program (Nutritionist IV, San Bruno, CA, USA) based on our own database. Restriction fragment length polymorphism of the estrogen-receptor-alpha gene was determined with the PvuII restriction enzyme. Obese women widely under-reported their daily food intake. The analysis of body fat distribution showed that the total body weight and the percentage of total fat mass were significantly increased in the obese group (p = 0.001). We observed significantly higher leptin (20.56 +/- 11.9 vs. 9.02 +/- 2.8 ng/ml) and total cholesterol (but lower cholesterol HDL), triglycerides levels in the obese subjects (261.89 +/- 48.8 vs. 248.23 +/- 55.9; 52.17 +/- 13.6 vs. 60.92 +/- 13.04; 142.82 +/- 61.02 vs. 106.61 +/- 27.7 mg/dl). Except for diastolic blood pressure, clinical variables were not significantly different between subjects with and without the PvuII ERalpha polymorphism. Allele frequencies of the ERalpha polymorphism did not differ from those previously reported (P-0.48, p-0.52) in our study. In this preliminary study we failed to find dietary and genetic factors involved in the pathogenesis of menopausal obesity. However, our results provide support for the notion that the perimenopausal increase in visceral fat is a significant factor involved in the increased cardiovascular risk in postmenopausal women.
这项初步研究探讨了与绝经后肥胖及其代谢后果发展相关的饮食、遗传和激素因素之间可能存在的关联。我们对43名未使用激素替代疗法（HRT）的绝经后女性进行了人体测量、激素和生化检测，并使用了一份营养调查问卷（14名肥胖女性和29名非肥胖女性，平均年龄±标准差为52.8±4.6岁，平均体重74.6±4.6千克）。所有女性还通过DPX-Lunar评估了脂肪量。根据24小时饮食回顾，使用基于我们自己数据库的计算机程序（美国加利福尼亚州圣布鲁诺的Nutritionist IV）计算每日食物定量中的营养摄入量。用PvuII限制性内切酶测定雌激素受体α基因的限制性片段长度多态性。肥胖女性普遍少报了她们的每日食物摄入量。体脂分布分析表明，肥胖组的总体重和总脂肪量百分比显著增加（p = 0.001）。我们观察到肥胖受试者的瘦素水平显著更高（20.56±11.9对9.02±2.8纳克/毫升），总胆固醇水平（但高密度脂蛋白胆固醇水平较低）、甘油三酯水平也更高（261.89±48.8对248.23±55.9；52.17±13.6对60.92±13.04；142.82±61.02对106.61±27.7毫克/分升）。除舒张压外，有无PvuII ERα多态性的受试者之间临床变量无显著差异。在我们的研究中，ERα多态性的等位基因频率与先前报道的无差异（P = 0.48，p = 0.52）。在这项初步研究中，我们未能发现参与绝经后肥胖发病机制的饮食和遗传因素。然而，我们的结果支持这样一种观点，即围绝经期内脏脂肪增加是绝经后女性心血管风险增加的一个重要因素。
