妊娠糖尿病患者肿瘤坏死因子的动态变化与胰岛素抵抗的关系
Alteration of serum tumor necrosis factor-alpha level in gestational diabetes mellitus and correlation with insulin resistance
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摘要: 目的 探讨妊娠糖尿病(GDM)患者肿瘤坏死因子α(TNF-α)的动态变化与胰岛素抵抗(IR)的关系.方法 选择GDM患者32例(GDM组)、正常孕妇31例(NGT组)为研究对象,分别测定孕25~28周、孕29~32周、孕37~38周、产后6~8周空腹血TNF-α、胰岛素、血糖水平,采用放射免疫法测定TNF-α和胰岛素,葡萄糖氧化酶法测定空腹血糖.以稳态模式评估法的胰岛素抵抗指数(HOMA-IR)评价IR.结果 ① GDM组、NGT组血清TNF-α水平均随孕期的增加而升高,且均显著高于产后;② GDM患者妊娠各时期TNF-α水平均显著高于NGT (t值分别为7.81、7.05、7.15,P<0.01);③血清TNF-α水平与HOMA-IR显著正相关(r=0.571,P<0.05).结论 GDM患者血清中TNF-α水平随孕期的增加而升高,且显著高于产后,TNF-α的动态变化与IR相关.Abstract: Objective To explore the dynamic of tumor necrosis factor-alpha(TNF-α)and its correlation with insulin resistance(IR)during different stages of gestational diabetes mellitus(GDM).Methods Thirty-two subjects with GDM and 31 cases of normal pregnant women nonnal glucose tolerance,NGT were enrolled in the study,serum TNF-α and insulin were determined by radioimmunoassay.The plasma glucose was measured by using glucose oxidase.Tests repeated for each group according different stages of prenatal 25~28 weeks,29~32 weeks,37~38 weeks and postpartum 6~8 weeks.IR was assessed by the homeostasis model of assessment for insulin resistance index(HOMA-IR).Results ① Serum TNF-α levels in GDM and NGT group rose with gestational age,and both significantly decreased at postpartum. ② Serum TNF-α levels in GDM of above-mentioned four stages respectively were(7.05±0.67)ng/L,(7.11±0.75)ng/L,(7.36±0.79)ng/L,(5.46±0.37)ng/L respectively.All significantly increased than those in the same stage group(t=7.81,7.05,7.15,P<0.01). ③ Maternal serum TNF-α levels were in positive correlation with HOMA-IR in GDM(r=0.571,P<0.05).Conclusions Serum TNF-α levels in GDM rose with gestational age,but significantly decreased at postpartum.The dynamic changes of serum TNF-α contribute to occurrence of insulin resistance.
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Key words:
- Diabetes, gestational /
- Tumor necrosis factor /
- Insulin resistance
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[1] 杨慧霞,张眉花,孙伟杰,等.妊娠糖代谢异常孕妇并发子痫前期的相关因素探讨.中华妇产科杂志,2005,,4(9):577-580.
[2] 胡春玲,罗毅平,李莉群,等.妊娠糖尿病与炎症因子关系的研究.江西医学学院学报,2006,46(2):62-65.
[3] Bloomgarden ZT. Inflammation and insulin resistance. Diabetes Care, 2003, 26(5):1619-1623. [4] 吴连芳.妊娠糖尿病的筛查与诊断.中华全科医师杂志,2005,4(8):462-463.
[5] Haffner SM, Miettinen H, Stern MP. The homeostasis model in the San Antonio Heart Study. Diabetes Care, 1997, 20(7):1087-1092. [6] 李旻,孙永玉.产科领域的胰岛素抵抗.国外医学妇幼保健分册,2003,14(2):65-68.
[7] Akbay E, Tiras MB, Yetkin I, et al. Insulin secretion and insulin sensitivity in normal pregnancy and gestational diabetes mellitus. Gynecol Endocrinol, 2003, 17(2):137-142. [8] Aderka D, Engelmamn H, Maor Y, et al. Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors. J Exp Med, 1992, 175(2):323-329. [9] Rui L, Aguirre V, Kim JK, et al. Insulin/IGF-1 and TNF-α stimulate phosphorylation of IRS-1 at inhibitory Ser307 via distinct pathways. J Clin Invest, 2001, 107(2):181-189. [10] BachaF, Saad R, Gungor N, et al. Adiponectin in youth:relationship to visceral adiposity, insulin sensitivity, and beta-cell function. Diabetes Care, 2004, 27(2):547-552. [11] Coughlan MT, Oliva K, Georgiou HM, et al. Glucose-induced release of tumour necrosis factor-alpha from human placental and adipose tissues in gestational diabetes mellitus. Diabet Med, 2001, 18(11):921-927. -
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