妊娠期糖尿病患者血清葡萄糖依赖性促胰岛素释放肽、成纤维细胞生长因子-23水平与产后糖代谢异常的关系

Correlations of serum glucose-dependent insulin releasing peptide and fibroblast growth factor-23 levels with abnormal postpartum glucose metabolism in patients with gestational diabetes mellitus

  • 摘要:
    目的 探讨妊娠期糖尿病(GDM)患者血清葡萄糖依赖性促胰岛素释放肽(GIP)、成纤维细胞生长因子-23(FGF23)水平与产后糖代谢异常的关系。
    方法 选取82例确诊GDM患者为研究对象, 并采集静脉血检测血清GIP、FGF23水平。产后12周采用75 g葡萄糖耐量试验(OGTT)评估患者糖代谢状态,并根据结果将GDM患者分为糖代谢正常组66例和糖代谢异常组16例。采用多因素Logistic回归模型分析影响GDM患者产后糖代谢异常的因素; 采用受试者工作特征(ROC)曲线分析血清GIP、FGF23预测GDM患者产后糖代谢异常的价值。
    结果 糖代谢异常组血清GIP水平低于糖代谢正常组, FGF23水平高于糖代谢正常组,差异有统计学意义(P < 0.01)。孕前高体质量指数(BMI)、高FGF23是GDM患者产后糖代谢异常的危险因素(P < 0.05), 高GIP是保护因素(P < 0.05)。GIP、FGF23、孕前BMI预测GDM患者产后糖代谢异常的曲线下面积(AUC)分别为0.717、0.625、0.699, GIP、FGF23、孕前BMI联合预测GDM患者产后糖代谢异常的AUC为0.890, 高于GIP、FGF23、孕前BMI单独预测价值(P < 0.05)。
    结论 GDM产后糖代谢紊乱患者血清GIP水平降低, FGF23水平增高,且与产后糖代谢异常有关。血清GIP和FGF23可预测GDM患者产后糖代谢异常风险。

     

    Abstract:
    Objective To explore the correlations of serum glucose-dependent insulin releasing peptide (GIP) and fibroblast growth factor-23 (FGF23) levels with abnormal postpartum glucose metabolism in patients with gestational diabetes mellitus (GDM).
    Methods A total of 82 patients with GDM were selected as research objects, and they were conducted with venous blood collection for detection of serum GIP and FGF23 levels. At 12 weeks after delivery, the 75 g oral glucose tolerance test (OGTT) was used to evaluate glucose metabolism status, and the GDM patients were divided into normal glucose metabolism group (n=66) and abnormal glucose metabolism group (n=16) according to the result of OGTT. Multivariate Logistic regression model was used to analyze the factors affecting abnormal postpartum glucose metabolism in GDM patients; the receiver operating characteristic (ROC) curve was used to analyze the values of serum GIP and FGF23 in predicting abnormal postpartum glucose metabolism in GDM patients.
    Results The serum GIP level in the abnormal glucose metabolism group was significantly lower than that in the normal glucose metabolism group, while the FGF23 level was significantly higher than that in the normal glucose metabolism group (P < 0.05). High pre-pregnancy body mass index (BMI) and high FGF23 were the risk factors for abnormal postpartum glucose metabolism in GDM patients, while high GIP was a protective factor (P < 0.05). The values of area under the curve (AUC) of GIP, FGF23 and pre-pregnancy BMI in predicting abnormal postpartum glucose metabolism in GDM patients were 0.717, 0.625 and 0.699 respectively, and the AUC of GIP combined with FGF23 and pre-pregnancy BMI in predicting abnormal postpartum glucose metabolism in GDM patients was 0.890, which was significantly higher than that of GIP, pre-pregnancy BMI or FGF23 alone (P < 0.05).
    Conclusion In GDM patients with abnormal postpartum glucose metabolism, serum GIP level reduces while FGF23 level increases, and these two indexes are related to abnormal postpartum glucose metabolism. Serum GIP and FGF23 can predict the risk of abnormal postpartum glucose metabolism in GDM patients.

     

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