Maternal Antioxidant Supplementation Prevents Adiposity in the Offspring of Western Diet–Fed Rats

  1. Rebecca A. Simmons1
  1. 1Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania;
  2. 2Division of Newborn Medicine, Tufts Medical Center, Boston, Massachusetts.
  1. Corresponding author: Rebecca A. Simmons, rsimmons{at}mail.med.upenn.edu.

Abstract

OBJECTIVE Obesity in pregnancy significantly increases the risk of the offspring developing obesity after birth. The aims of this study were to test the hypothesis that maternal obesity increases oxidative stress during fetal development, and to determine whether administration of an antioxidant supplement to pregnant Western diet-fed rats would prevent the development of adiposity in the offspring.

RESEARCH DESIGN AND METHODS Female Sprague Dawley rats were started on the designated diet at 4 weeks of age. Four groups of animals were studied: control chow (control); control + antioxidants (control+Aox); Western diet (Western); and Western diet + antioxidants (Western+Aox). The rats were mated at 12 to 14 weeks of age, and all pups were weaned onto control diet.

RESULTS Offspring from dams fed the Western diet had significantly increased adiposity as early as 2 weeks of age as well as impaired glucose tolerance compared with offspring of dams fed a control diet. Inflammation and oxidative stress were increased in preimplantation embryos, fetuses, and newborns of Western diet-fed rats. Gene expression of proadipogenic and lipogenic genes was altered in fat tissue of rats at 2 weeks and 2 months of age. The addition of an antioxidant supplement decreased adiposity and normalized glucose tolerance.

CONCLUSIONS Inflammation and oxidative stress appear to play a key role in the development of increased adiposity in the offspring of Western diet-fed pregnant dams. Restoration of the antioxidant balance during pregnancy in the Western diet-fed dam is associated with decreased adiposity in offspring.

Footnotes

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  • Received March 2, 2010.
  • Accepted August 20, 2010.

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  1. Diabetes vol. 59 no. 12 3058-3065
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