In non-pregnant obese subjects, elevated circulating adipose-derived pro-inflammatory cytokines contribute to insulin resistance. We hypothesise that in pregnancy, a state of progressive insulin resistance, obesity significantly reduces adipose insulin sensitivity thus enhancing lipolysis in the third trimester.
We carried out hyperinsulinaemic euglycaemic clamp studies in healthy morbidly obese (BMI>40kg/m2; n=9) and lean (BMI<25kg/m2; n=6) pregnant women at 19 and 36 weeks gestation, and in morbidly obese and lean non-pregnant women (n=7 per group). Whole body steady state glucose disposal (mg/kg/min) was used as a surrogate measure of insulin sensitivity (IS). Fasting blood and subcutaneous adipose tissue were obtained; pro-inflammatory cytokines, adipokines and free fatty acids were quantified.
At 19 weeks gestation, IS was significantly greater in lean compared with obese pregnant women (8.4±1.4 vs 2.9±0.3 mg/kg/min, p<0.001). There was an approximately 50% decrement in IS in lean women by 36 weeks, however, there was no such decrement in obese women. By 36 weeks gestation, there was no difference in insulin sensitivity between lean and obese pregnant women. Serum NEFA were higher in obese compared with lean women at 19 weeks (0.53±0.03 vs 0.33±0.03mmol/L, p<0.05) but again there was no significant difference between lean and obese pregnant women by 36 weeks gestation.
We conclude that, in contrast to lean women, pregnancy is not associated with a decline in IS in morbidly obese pregnant women and that it may be prolonged exposure to an insulin resistant environment rather than the severity of insulin resistance which contributes to the pathogenesis of obesity-associated complications.
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