INFLUENCE OF MATERNAL OBESITY ON INSULIN SENSITIVITY AND SECRETION IN THE OFFSPRING

Abstract

Objective: To clarify the effects of maternal obesity on insulin sensitivity and secretion in the offspring.

Research Design And Methods: Fifty-one offspring of both sexes of obese (Ob) and 15 offspring of normal weight (C) mothers were studied. Plasma glucose, insulin and C-peptide were measured during an OGTT. Insulin sensitivity was calculated using the Oral Glucose Insulin Sensitivity (OGIS) index and insulin secretion and beta-cell glucose sensitivity were computed by a mathematical model. Fasting leptin and adiponectin were also measured. Body composition was assessed by Dual-X-ray Absorptiometry.

Results: No birth weight statistical difference was observed in the two groups. Sixty-nine % of the Ob offspring were obese and 19% were overweight. Ob were more insulin resistant than C subjects (398.58±79.32 vs. 513.81±70.70 ml·min⁻¹m⁻² in women, P<0.0001 and 416.42±76.17 vs. 484.242±45.76 ml·min⁻¹m⁻² in men P<0.05). Insulin secretion after OGTT was higher in Ob than in C men (63.94±21.20 vs. 35.71±10.02 nmol·m⁻², P<0.01), but did not differ significantly in women. Beta-cell glucose sensitivity was not statistically different between groups. A multivariate analysis of variance showed that maternal obesity and offspring gender concurred together with BMI and beta-cell glucose sensitivity to determine the differences in insulin sensitivity and secretion observed in the offspring.

Conclusions: Obese mothers can give birth to normal birth weight babies who later develop obesity and insulin resistance. The maternal genetic/epigenetic transmission shows a clear sexual dimorphism, with male having a higher value of insulin sensitivity (although not statistically significant) associated with a significantly higher insulin secretion than female offspring.