Objective: To test the hypothesis that gravidas who have an abnormal response to glucose loading have dysfunctional adipose tissue cells that produce more insulin resistance-inducing and proinflammatory adipokines but less insulin-sensitizing adipokines.
Methods: We performed a nested case-control study within a larger sample of gravidas who had a glucose challenge test (GCT) at 24-29 weeks; we compared 73 cases with an abnormal GCT (>8.3 mM) and 146 controls with a strictly normal GCT (<7.2 mM) matched for body mass index (BMI) and height (mean difference between cases and controls: 0.1 kg/m(2) and 1 cm, respectively). We measured plasma insulin, adipokines (leptin, adiponectin, resistin, tumor necrosis factor [TNF]-alpha, interleukin [IL]-6), soluble leptin receptor (sOb-R), the main leptin-binding protein, and C-reactive protein (CRP).
Results: The cases showed a 48% increase in insulin concentrations and a 27% increase in TNF-alpha concentrations compared to the controls (both P < .0001), but leptin, sOb-R, IL-6, and adiponectin, as well as CRP, concentrations were comparable between cases and controls. In the whole group (n = 219), BMI was correlated with insulin, leptin, IL-6, and CRP, and inversely with sOb-R and adiponectin concentrations (all P < .0003).
Conclusions: Plasma leptin, sOb-R, IL-6, and adiponectin, as well as CRP, are strongly related to BMI in gravidas at 24-29 weeks gestational age but not to the glucose loading response. However, TNF-alpha is higher in women with an abnormal GCT. Further studies should disclose the source of increased TNF-alpha in these women, and to assess whether TNF-alpha is causally related to glucose intolerance during pregnancy.