Beta-cell function and insulin resistance in pregnancy and their relation to fetal development

Insulin resistance in pregnancy is consequent to the physiological adaptation necessary to provide glucose to the growing fetus. Disturbance in the maternal metabolism can induce structural and functional adaptations during fetal development.

Pregnant women with duration of conception between 24 and 28 weeks were assessed for insulin resistance (IR) and beta-cell function by using homeostatic model assessment IR (HOMA-IR) and homeostatic model assessment of beta-cell function (HOMA-B) models, respectively. One hundred pregnant women and 42 age-matched controls were taken for the study. Fourteen pregnant women were diagnosed as gestational diabetes mellitus (GDM) as per World Health Organization (WHO) criteria.

Pregnant women with normal glucose tolerance (NGT) did not reveal significant IR as compared to controls but the HOMA-B was higher (268.91 +/- 197.16 vs 188.6 +/- 88.83, P < 0.01), suggesting excessive beta-cell function to maintain glucose homeostasis. The subset of pregnant women who presented with GDM had significantly higher HOMA-IR values (6.59 +/- 2.93 vs. 1.77 +/- 1.49, P < 0.001) and similar HOMA-B values as compared to pregnant women with NGT. Pregnant women with severe IR manifested as GDM, even without any previous history of dysglycemia.

With regard to fetal outcome, HOMA-IR is an independent predictor in pregnant women with NGT (biparietal diameter r(2) = 0.204, P < 0.01; weight r(2) = 0.097, P < 0.01), whereas beta-cell function (HOMA-B) is a strong independent predictor of fetal outcome in pregnant GDM (biparietal diameter r(2) = 0.58, P < 0.05; FL r(2) = 0.71, P < 0.01 AC r(2) = 0.79, P < 0.001; weight r(2) = 0.57, P < 0.01).