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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #241905
Title: Maternal obesity during conception programs offspring's body composition: Modulation of fatty acid synthase expression

Author
item SHANKAR, KARTIK - Arkansas Children'S Nutrition Research Center (ACNC)
item HARRELL, AMANDA - Arkansas Children'S Nutrition Research Center (ACNC)
item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)
item BADGER, THOMAS - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Obesity
Publication Type: Abstract Only
Publication Acceptance Date: 6/30/2008
Publication Date: 10/15/2008
Citation: Shankar, K., Harrell, A., Ronis, M.J., Badger, T.M. 2008. Maternal obesity during conception programs offspring's body composition: Modulation of fatty acid synthase expression [abstract]. Obesity. 16(S1):502P.

Interpretive Summary:

Technical Abstract: The risk of obesity in later 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 by intragastric feeding of diets using total enteral nutrition. Feeding liquid diets to female SD rats at 220 kcal/kg3/4/d (15% excess calories/d) compared to 187 kcal/kg3/4/d (NRC requirements) for 3 wk caused substantial increase in body-weight (BW) gain, adiposity, serum insulin, leptin and insulin resistance. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups at birth. Numbers of pups, birth weight, and size were not affected by maternal obesity. Obese dam offspring when weaned on high-fat diets (HFD, 45% fat calories) gain significantly greater BW, adiposity (via EchoMRI and LaTheta CT scanning), and insulin resistance (oral glucose tolerance tests) than lean dam offspring on the same diet. Metabolic and hormonal parameters were measured in the offspring. Histomorphometry revealed greater adipose hypertrophy in offspring of obese dams. To examine the underlying mechanisms of obesity-induced programming, we examined levels of fatty acid synthase (FAS) gene and protein expression in the retroperitoneal adipose tissue of the offspring. Consumption of HFD in the offspring of lean dams increased FAS protein levels (about 5-fold, p<0.05). However, induction of FAS protein in the offspring of obese dams was about 3-fold greater than that observed in the lean dam counterparts on the same diet (p<0.0001). In addition, mRNA levels of FAS were greater in the offspring of obese dams compared to lean dams (p<0.05). Hepatic FAS and acetyl CoA carboxylase (ACC) protein levels were induced (p<0.05) in offspring of obese rats, while phosphorylated ACC levels did not differ between groups. These data suggest that maternal obesity leads to fetal programming of the offspring in later-life upon challenge with an obesegenic diet via modulation of lipogenic gene induction.