脂肪因子与妊娠期糖尿病胰岛素抵抗的相关性研究

目的了解妊娠期糖尿病（GDM）孕妇血清脂肪细胞因子内脂素、脂联素、肿瘤坏死因子-α表达水平的变化，探讨其与妊娠期糖尿病胰岛素抵抗的相关性。方法选择2008年12月-2009年3月在复旦大学附属妇产科医院产科门诊行常规产前检查并足月入院待产的孕妇。其中正常对照组22例，GDM组20例。检测人体测量参数和生化指标。采用ELISA方法检测两组血清内脂素、脂联素、肿瘤坏死因子-α（TNF-α）水平。用最小稳态模型计算胰岛素抵抗指数（HOMA—IR）：空腹血糖（FPG）×空腹胰岛素（FINS）／22．5。结果（1）GDM组血清内脂素（[7．9±2．0]vs[6．2±1．4]ng／ml，P〈0．01）与TNF-α（90．0±30．0）vs[53．7±48．0]pg／ml，P〈0．01）水平显著高于正常对照组。而GDM组血清脂联素水平较正常对照组明显下降（[309．0±210．4]vs[584．9±419．4]Pg／ml，P〈0．05）。（2）研究对象总体中内脂素与餐后1h血糖（1hPG）呈显著正相关（r=0．432，P=0．004），而与脂联素呈明显负相关（r=-0．374，P=0．015）。脂联素与1hPG及内脂素呈显著负相关（r=-0．442，P=0．003；r=-0．374，P=0．015）。TNF—α与FINS、HOMA-IR呈显著正相关（r=0．376，P=0．014；r=0．320，P：0．039）（3）多因素Logistic逐步回归分析结果显示排除1hPG影响后GDM与脂联素（B=-0．030，P=0．041，OR=0．997，95％CI0．993—1．000）呈显著负相关，与FINS（B=0．620，P=0．029，OR=1．859，95％CI1．067—3．239）呈显著正相关。进一步校正FINS后内脂素（B=0．527，P=0．042，OR=1．694，95％CI1．020～2．815）、TNF-α（B=0．036,P=0．008，OR=1．037，95％CI1．010—1．065）成为GDM的独立影响因子。结论妊娠糖尿病孕妇血清内脂素、脂联素和TNF-α水平的改变与妊娠期胰岛素抵抗有关并可能通过不同的作用途径参与妊娠期糖尿病的发生和发展。

The relationship between adipocytokins and insulin resistance of women with gestational diabetes mellitus.

Objective： To investigate the changes of serum visfatin, adiponectin and TNF - α levels in women with gestational diabetes mellitus （GDM） and their association with insulin resistance. Methods ： Samples for measurement were obtained from 20 women with GDM and 22 healthy pregnant controls at term. Serum visfatin, adiponectin and TNF - α levels were detected by ELISA. The HOMA -insulin resistance index （HOMA -IR） was calculated based on fasting plasma glucose （FPG） and fasting blood insulin （FINS） with the minimal model. Results： （1） Compared with the normal pregnant controls, serum visfatin concentration （ [ 7. 9 ± 2.0] vs [ 6.2±1.4] ng/ml, P 〈 0.01） and TNF-α level （[90.0±30.0] vs [ 53.7±48.0] pg/ml, P 〈 0.01） were significantly elevated in women with GDM. At the same time, serum adiponection levels was significantly lower in women with GDM than healthy pregnant controls （ [309.0 ±210. 4] vs [ 584.9±419.4] pg/ml, P 〈 0. 05）. （2） In the whole group studied, serum visfatin level correlated positively with 1 h plasma glucose after glucose loading （ 1 hPG, r = 0. 432, P = 0. 004） and negatively with adiponectin （ r = -0. 374, P =0. 015）. Serum adiponectin concentration correlated negatively with lhPG and visfatin （ r = -0. 442, P = 0. 003; r = -0. 374, P = 0. 015）. Serum TNF -α level correlated positively with FINS and HOMA -IR （ r = 0. 376, P = 0. 014 ; r = 0. 320, P = 0. 039）. （3） Data from multivariate analysis showed that GDM was significantly negatively correlated with adiponectin （ B = - 0. 030, P = 0. 041, OR = 0. 997, 95% CI 0. 993 -1. 000） and positively associated with FINS （ B = 0. 620, P = 0.029, OR =1.859, 95%CI 1.067 -3.239） after correcting lhPG. After further correcting FINS, Visfatin （B =0.527, P = 0. 042, OR = 1. 694, 95% CI 1. 020 - 2. 815） and TNF - α （B = 0. 036, P = 0. 008, OR = 1. 037, 95% CI 1. 010-1. 065） were independent related factors of GDM. Conclusions： Visfatin, adiponectin and TNF - α may be associated with insulin resistance in women with GDM and contribute through different ways.