Diet-induced obesity in gravid rats engenders early hyperadiposity in the offspring.

Exposure to a dysmetabolic in utero environment may be one of the mechanisms to explain why individuals with high birth weight are more likely to remain overweight. We explored this hypothesis in an animal model of diet-induced obesity (DIO). We studied adipose tissue development and glucose tolerance in the offspring of rat dams fed a diet rich in milk and sugar from early adulthood until day (d) 2 postpartum. This diet promoted body weight (BW) gain and was previously shown to produce insulin resistance and gestational glucose intolerance. The DIO offspring showed a higher BW in early life (between d7 and d35), with a maximum of 1 SD above the mean BW of controls; however, BW in DIO offspring after d35 was comparable with that of controls. Neonatal DIO offspring also showed larger fat depots, adipocyte hypertrophy (P <or= .001), and more than 2-fold increased tumor necrosis factor alpha messenger RNA levels in subcutaneous adipose tissue (P < .05). In addition, they displayed a higher peak glucose response to a glucose challenge (P < .05). In postpubertal (d56) and adult (d98) offspring, we found differences in fat mass and distribution and glucose tolerance relating to the offspring's sex but not the maternal diet. In conclusion, DIO during pregnancy results in hyperadiposity and reduced glucose tolerance only in their neonatal/weanling but not postpubertal offspring. Future research should disclose whether these early-life effects are reactivated in conditions of heightened insulin resistance.