Impaired beta-cell function in lean normotolerant former gestational diabetic women

Former gestational diabetes (fGDM) constitutes a risk condition for the development of Type 2 diabetes. Former gestational diabetes is often characterized by obesity and hyperglycaemia, which may be concomitant and independent risk factors.

To assess insulin sensitivity and beta-cell function in fGDM uncomplicated by obesity and hyperglycaemia, we studied 24 lean fGDM women and 23 control women matched for age (30.7 +/- 0.7 years, whole cohort), body mass index (22.2 +/- 0.3 kg m(-2)), and indistinguishable for plasma glucose both at fasting and at 120 min. Several insulin sensitivity and beta-cell function indices were computed: homeostasis model assessment insulin resistance index (HOMA-R), insulin sensitivity index derived from an oral glucose tolerance test (OGIS), insulinogenic index, other empirical indices of insulin secretion and beta-cell function, and indices obtained using a beta-cell model.

Though the majority of indices, and in particular insulin sensitivity (HOMA-R: 1.35 +/- 0.13 vs. 1.65 +/- 0.14; OGIS: 492.7 +/- 6.3 vs. 496.4 +/- 9.4 mL min(-1) m(-2)), were not significantly different in the two groups, the beta-cell glucose sensitivity obtained by modelling analysis was lower in fGDM (108 +/- 14 vs. 165 +/- 22 pmol min(-1) m(-2) mM(-1), P = 0.031).

Impairment of beta-cell glucose sensitivity may be an intrinsic risk factor in fGDM independently of obesity and hyperglycaemia. Furthermore, we have shown that modelling analysis, in contrast to the empirical parameters, may be able to detect early beta-cell alterations in fGDM women.