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Am J Physiol Regul Integr Comp Physiol 293: R2006-R2012, 2007. First published August 29, 2007; doi:10.1152/ajpregu.00382.2007
0363-6119/07 $8.00
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DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Neonatal dietary supplementation of arachidonic acid increases prostaglandin levels in adipose tissue but does not promote fat mass development in guinea pigs

Olivier Aprikian,1 Denis Reynaud,2 Cecil Pace-Asciak,2 Patricia Leone,1 Florence Blancher,1 Irina Monnard,1 Christian Darimont,1 and Katherine Macé

1Nestlé Research Centre, Lausanne, Switzerland; and 2Research Institute, The Hospital for Sick Children, Toronto, Canada

Submitted 31 May 2007 ; accepted in final form 24 August 2007

The role of arachidonic acid (AA) on the development of adipose tissue is still controversial since its metabolites, i.e., prostaglandins, can either stimulate or inhibit preadipocyte differentiation in vitro. In the present study, we evaluated the effects of early postnatal supplementation of AA on body weight and adipose tissue development in guinea pigs. Male newborn guinea pigs were fed for 21 days (day 21) with diets (milk and pellet) supplemented (+AA) or not (–AA) with 1.2% (total fatty acids) AA. From day 21 to day 105 both groups were fed a chow diet. The 21-days-old +AA pups showed a twofold higher AA accretion in phospholipids associated with a two- to sixfold increase in several prostaglandins, such as 6-keto PGF1{alpha} (the stable hydrolysis product of PGI2), PGF2{alpha}, PGE2, and PGD2 in adipose tissue, compared with the –AA group. No difference in fat pad and body weight, aP2, and leptin gene expression in adipose tissue, fasting plasma glucose, free-fatty acids, and triglyceride concentration was observed between groups at day 21 or day 105. These results show that dietary supplementation of AA during the suckling/weaning period increases prostaglandin levels in adipose tissue but does not influence early fat mass development in the guinea pig.

dietary fat; polyunsaturated fatty acids; eicosanoids; metabolic programming; obesity



Address for reprint requests and other correspondence: K. Macé, Nestlé Research Centre, PO Box 44, Vers-Chez-Les-Blanc, 1000 Lausanne 26, Switzerland (e-mail: catherine.mace{at}rdls.nestle.com)







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