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Title: Maternal Obesity at Conception Programs Obesity in the Offspring


Submitted to: American Journal of Physiology - Regulatory Integrative & Comparative Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/19/2007
Publication Date: 2/1/2008
Citation: Shankar, K., Harrell, A., Liu, X., Gilchrist, J.M., Ronis, M.J., Badger, T.M. 2008. Maternal obesity at conception programs obesity in the offspring. American Journal of Physiology - Regulatory Integrative & Comparative Physiology. 294(2):R528-38.

Interpretive Summary: As the prevalence of obesity among pregnant women continues to rise, greater numbers of children are exposed to an 'obese intrauterine environment during development. We have examined the central question of whether in utero exposure to maternal obesity increases the risk of obesity in the offspring in later-life. To this end, we have developed an overfeeding-based model of maternal obesity in a genetically homogenous population of rats by intragastric feeding of diets using total enteral nutrition. Using this model we have attempted to dissect the fetal programming imposed by maternal obesity via metabolic factors independent of genetic influences. Despite no differences in body-weights at birth or weaning, offspring of obese dams when weaned to an ad libitum high-fat obesegenic diet, showed remarkable body-weight and adiposity increases compared to cohorts of offspring from lean dams fed the same diet. These findings suggest that maternal obesity during gestation alone is sufficient to increase the susceptibility of the offspring to obesity.

Technical Abstract: The risk of obesity in adult-life is subject to programming during gestation. To examine whether in utero exposure to maternal obesity increases the risk of obesity in the offspring, we have developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition (TEN). Feeding liquid diets to adult female rats at 220 kcal/kg3/4/d (15% excess calories/d) compared to 187 kcal/kg3/4/d for 3 wk caused substantial increase in body-weight gain, adiposity, serum insulin, leptin, and insulin resistance. Lean or obese female rats were mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Numbers of pups, birth weight and size were not affected by maternal obesity. Male offspring from each group were weaned at PND21 to either AIN-93G diets or high fat diets (HFD, 45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese dams gained remarkably greater (p < 0.005) body weight and higher percent body fat when fed HFD. Body composition was assessed by NMR, X-ray computerized tomography, and weights of adipose tissues. Adipose histomorphometry, insulin sensitivity and food intake were also assessed in the offspring. Our data suggest that maternal obesity at conception leads to fetal programming of the offspring that could result in obesity in later-life.