4.4 Article

Do adiponectin, TNFα, leptin and CRP retate to insulin resistance in pregnancy?: Studies in women with and without gestational diabetes, during and after pregnancy

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DIABETES-METABOLISM RESEARCH AND REVIEWS
卷 22, 期 2, 页码 131-138

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WILEY
DOI: 10.1002/dmrr.591

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gestational diabetes; adipocytokines; pregnancy; insulin resistance; insulin secretion

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Background The role of adiponectin, tumour necrosis factor alpha (TNF alpha), leptin and C-reactive protein in the insulin resistance of pregnancy is not clear. We measured their levels in women with gestational diabetes (GDM) and in controls, during and after pregnancy, and related them to insulin secretion and action. Methods Nineteen women with GDM and 19 BMI-matched healthy pregnant women underwent intravenous glucose tolerance tests in the third trimester of pregnancy and 4 months postpartum to determine insulin sensitivity (SI) and insulin secretion. Adiponectin, TNF alpha, leptin and high sensitivity CRP (hsCRP) were measured in fasted blood. only leptin (r = -0.41, p = 0.01) Results Of the circulating factors, correlated with SI in pregnancy. Leptin and hsCRP levels were elevated in pregnancy compared to postpartum (leptin (mean +/- SEM): 27.8 +/- 2.4 vs 19.3 +/- 2.1 ng/mL, p < 0.001; hsCRP: 5.2 +/- 0.7 vs 3.2 +/- 0.6 mg/L, p < 0.001). Adiponectin levels did not change from pregnancy to postpartum, despite a marked increase in SI. All four factors correlated with SI postpartum (adiponectin: r = 0.38, p = 0.01; TNFa: r = -0.48, p = 0.002; Leptin: r = - 0. 6 1, p = 0. 00 1; hsCRP: r = - 0. 48, p = 0. 002). TNFa correlated inversely with insulin secretion in pregnancy (r=-0.35,p=0.03) and was significantly higher in the GDM group (2.62 +/- 0.3 vs 1.88 +/- 0.3 pg/mL, p = 0.01) in pregnancy. Conclusion In our study, the influence of adiponectin, TNFa and hsCRP upon SI is overwhelmed by other factors in pregnancy. While leptin and SI correlated in pregnancy, it is unclear whether this represents cause or effect. Finally, TNFa may exert an inhibitory effect on insulin secretion in GDM, contributing to the associated hyperglycaemia. Copyright (c) 2005 John Wiley & Sons, Ltd.

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