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1 Arkansas Children's Nutrition Center, Little Rock, Arkansas, United States; Pharmacology & Toxicology, University of Arkansas for Medical Sciences
2 Arkansas Children's Nutrition Center, Little Rock, Arkansas, United States
3 Arkansas Children's Nutrition Center, Little Rock, Arkansas, United States; Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
4 Arkansas Children's Nutrition Center, Little Rock, Arkansas, United States; Department of Physiology/Biophysics, University of Arkansas for Medical Science, Little Rock,, Arkansas, United States; Pharmacology & Toxicology, University of Arkansas for Medical Sciences
* To whom correspondence should be addressed. E-mail: ShankarKartik{at}uams.edu.
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 %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.
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