Objective: The purpose of this study was to clarify the effects of maternal obesity on insulin sensitivity and secretion in offspring.
Research design and methods: Fifty-one offspring of both sexes of obese (Ob group) and 15 offspring of normal-weight (control group) mothers were studied. Plasma glucose, insulin, and C-peptide were measured during an oral glucose tolerance test (OGTT). Insulin sensitivity was calculated using the oral glucose insulin sensitivity 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. Of the Ob group, 69% were obese and 19% were overweight. The Ob group were more insulin resistant than the control group (398.58 +/- 79.32 vs. 513.81 +/- 70.70 ml(-1) x min(-1) x m(-2) in women, P < 0.0001; 416.42 +/- 76.17 vs. 484.242 +/- 45.76 ml(-1) x min(-1) x m(-2) in men, P < 0.05). Insulin secretion after OGTT was higher in Ob group than in control group men (63.94 +/- 21.20 vs. 35.71 +/- 10.02 nmol x 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 sex concurred together with BMI and beta-cell glucose sensitivity to determine the differences in insulin sensitivity and secretion observed in 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 offspring having a higher value of insulin sensitivity (although not statistically significant) associated with significantly higher insulin secretion than female offspring.