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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #213653
Title: Fetal programming by maternal obesity increases offspring’s susceptibility to obesity in later-life

Author
item SHANKAR, KARTIK - ACNC/UAMS
item LIU, XIAOLI - ACNC/UAMS
item HARRELL, AMANDA - ACNC
item RONIS, MARTIN - ACNC/UAMS
item BADGER, THOMAS - ACNC/UAMS

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 1/15/2007
Publication Date: 4/28/2007
Citation: Shankar, K., Liu, X., Harrell, A., Ronis, M.J., Badger, T.M. 2007. Fetal programming by maternal obesity increases offspring's susceptibility to obesity in later-life [abstract]. The FASEB Journal. 21(5):A324.

Interpretive Summary: The rise in the incidence of childhood obesity has been steep over the past two decades. We tested the hypothesis that this rapid increase was due in part to the influence of mother’s body composition on fetal development. We thought that overweight women might produce signals that would transfer to their fetus and these signal could establish changes in the development of their offspring which would later result in the overweight offspring. This is called fetal programming, because the signals from the pregnant women programmed the way offspring respond to foods later in life. This study in rats showed that if rats were obese at conception, their offspring became more obese later in life than offspring from lean moms, even though their genetics were identical. This is an important discovery and will be the topic of much future research at the ACNC.

Technical Abstract: To examine whether exposure of the developing fetus to an obese mother during pregnancy increases the risk of obesity in the children in later-life, we have developed an overfeeding-based model of maternal obesity in rats by tube feeding of liquid diets directly into the stomach using total enteral nutrition. Feeding liquid diets containing 15% excess calories to female SD rats at for 3 wks caused substantial increase in body-weight gain, fat tissue, serum insulin, leptin and insulin resistance. Lean or obese female rats were mated with control male rats. Exposure to obesity was ensured to be limited only to pregnancy by cross-fostering pups to non-cannulated lean dams with unrestricted access to control diets throughout lactation. Numbers of pups, birth weight and size were not affected by maternal obesity. Male offspring from each group were weaned at post-natal day (PND)21 to either control diets or high density/high fat diets (HFD, 45% fat calories). Monitoring weekly body-weights until PND130, revealed that while body weights of pups from obese mothers did not differ from pups of lean mothers on AIN-93G diets, pups from obese mothers gained remarkably greater (p<0.05) body weights and had a higher fat to body weight ratio on a HFD. Average body weights at PND130 were 800 +/- 26 g for the HFD pups from obese mothers vs. 683 +/- 22 g for HFD-pups from lean mothers. Body composition was assessed by EchoMRI, LaTheta CT scanning and weights of adipose tissues. Metabolic and hormonal parameters were also measured in the pups. These data suggest that maternal obesity may lead to programming of children's body composition that could result in obesity on challenge with a high calorie, high fat diet in later-life.