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




The role of adiponectin, tumour necrosis factor α (TNFα), 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.


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, TNFα, leptin and high sensitivity CRP (hsCRP) were measured in fasted blood.


Of the circulating factors, only leptin (r = −0.41, p = 0.01) 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; TNFα: r = −0.48, p = 0.002; Leptin: r = −0.61, p = 0.001; hsCRP: r = −0.48, p = 0.002). TNFα 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.


In our study, the influence of adiponectin, TNFα 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, TNFα may exert an inhibitory effect on insulin secretion in GDM, contributing to the associated hyperglycaemia. Copyright © 2005 John Wiley & Sons, Ltd.