Maternal docosahexaenoic acid increases adiponectin and normalizes IUGR-induced changes in rat adipose deposition. J Obes 2013;2013:312153
Date
03/28/2013Pubmed ID
23533720Pubmed Central ID
PMC3606778DOI
10.1155/2013/312153Scopus ID
2-s2.0-84875459534 (requires institutional sign-in at Scopus site) 25 CitationsAbstract
Intrauterine growth restriction (IUGR) predisposes to obesity and adipose dysfunction. We previously demonstrated IUGR-induced increased visceral adipose deposition and dysregulated expression of peroxisome proliferator activated receptor- γ 2 (PPAR γ 2) in male adolescent rats, prior to the onset of obesity. In other studies, activation of PPAR γ increases subcutaneous adiponectin expression and normalizes visceral adipose deposition. We hypothesized that maternal supplementation with docosahexaenoic acid (DHA), a PPAR γ agonist, would normalize IUGR adipose deposition in association with increased PPAR γ , adiponectin, and adiponectin receptor expression in subcutaneous adipose. To test these hypotheses, we used a well-characterized model of uteroplacental-insufficiency-(UPI-) induced IUGR in the rat with maternal DHA supplementation. Our primary findings were that maternal DHA supplementation during rat pregnancy and lactation (1) normalizes IUGR-induced changes in adipose deposition and visceral PPAR γ expression in male rats and (2) increases serum adiponectin, as well as adipose expression of adiponectin and adiponectin receptors in former IUGR rats. Our novel findings suggest that maternal DHA supplementation may normalize adipose dysfunction and promote adiponectin-induced improvements in metabolic function in IUGR.
Author List
Bagley HN, Wang Y, Campbell MS, Yu X, Lane RH, Joss-Moore LAMESH terms used to index this publication - Major topics in bold
AdiponectinAdipose Tissue
Animals
Dietary Supplements
Docosahexaenoic Acids
Female
Fetal Growth Retardation
Male
Maternal-Fetal Exchange
PPAR gamma
Pregnancy
RNA, Messenger
Rats
Receptors, Adiponectin
Subcutaneous Fat
