机构地区:[1]中国医学科学院北京协和医学院北京协和医院内分泌科国家卫生和计划生育委员会内分泌重点实验室,100730
出 处:《中华临床营养杂志》2015年第4期209-213,共5页Chinese Journal of Clinical Nutrition
基 金:国家l临床重点专科建设项目(WBYWBYZ2011-873);北京市自然科学基金(7122144)
摘 要:目的分析糖代谢异常孕妇与糖代谢正常孕妇早中孕期体质量增加的差异。方法回顾性分析2010年1月至2011年5月在北京协和医院就诊的孕妇,收集妊娠期糖代谢异常和正常孕妇早中孕期体质量增加、孕前体质量指数(BMI)、中孕末期BMI、年龄、肥胖史、糖尿病家族史、口服葡萄糖耐量试验(OGTT)胰岛素水平、血脂水平等数据。结果共216例糖代谢异常患者(病例组)和230名同期糖代谢正常孕妇(对照组)纳入研究。病例组早中孕期体质量增加量为10.0(8.1,12.5)kg,BMI增加值为(4.01±1.43)ks/m2,中孕期末BMI为(25.84±3.14)ks/m2;对照组早中孕期体质量增加量为9.5(7.0,11.5)kg,BMI增加值为(3.60±1.43)ks/m2,中孕期末BMI为(25.10±3.00)ks/m2;病例组均高于对照组,差异均有统计学意义(均P〈0.05)。病例组孕前BMI高于对照组[(21.84±2.99)kg/m2比(21.50±2.82)kg/m2],但差异无统计学意义(P〉0.05)。同时,与对照组相比,病例组年龄较大[(33.17±3.65)岁比(31.68±3.36)岁],有较高的空腹胰岛素水平[11.2(7.1,16.3)mU/L比8.9(6.5,13.7)mU/L]、服糖后峰值胰岛素水平[135.3(99.7,208.0)mU/L比104.9(75.6,144.4)mU/L]、稳态模型法评估胰岛素抵抗指数(HOMA—IR)[2.40(1.49,3.47)比1.82(1.28,2.71)]、三酰甘油[2.62(2.04,3.31)mmol/L比2.18(1.81,2.81)mmol/L],差异均有统计学意义(均P〈0.05)。而两组间既往肥胖史、糖尿病家族史、月经紊乱史则差异无统计学意义(均P〉0.05)。结论糖代谢异常孕妇比糖代谢正常孕妇早中孕期体质量增长较多,早中孕期体质量增长过多可能是发生妊娠糖代谢异常的危险因素。Objective To study the difference of body weight gain in the first and second trimesters between pregnant women with abnormal gestational glucose metabolism and those with normal gestational glucose metabolism. Methods We retrospectively analyzed the data of pregnant women visited the obstetric clinic of Peking Union Medical College Hospital from January 2010 to May 2011, with or without abnormal glucose metabolism. The data of body weight gain in the first and second trimesters, body mass index (BMI) before preg- nancy, BMI in the end of second trimester, age, obesity history, diabetes family history, insulin level in the oral glucose tolerance test ( OGTT), and lipid profile of these women were collected. Results Altogether 216 pregnant women with abnormal glucose metabolism ( case group) and 230 pregnant women with normal glucose metabolism (control group) were included in this study. In the case group, the increment of body weight in the first and second trimesters was 10. 0 (8. 1, 12. 5) kg, and the increment of BMI was (4. 01 +- 1.43) kg/m2, BMI in the end of the second trimester was (25.84 +- 3.14) kg/m2 ; in comparison, the increments of body weight and BMI in the first and second trimesters were 9. 5 (7.0, 11.5 ) kg and (3.60 +- 1.43 ) kg/m2, respectively, BMI in the end of the second trimester was (25.1 + 3.00) kg/m2 in the control group, all significantly lower than in the case group ( all P 〈 0. 05 ). The BMI before pregnancy was higher in the case group than in the control group [ (21.84 +-2. 99) kg/m2 vs. (21.50 +-2. 82) kg/m2], but with no statistical signifi- cance (P 〉0. 05). Compare with the control group, the case group had older age [ (33. 17 +-5.65) years vs. (31.68 +-3.36) years], higher fasting insulin level [ 11.2 (7.1, 16. 3) mU/L vs. 8.9 (6. 5, 13.7) mU/L], higher peak insulin level in OGTT [ 135.3 (99. 7, 208.0) mU/L vs. 104. 9 (75.6, 144. 4) mU/L] , higher homeostasis model assessment fo
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