MS

thesisIntrauterine growth restriction (IUGR) increases the risk of obesity and insulin resistance in adulthood. Insulin resistance is inversely correlated with serum adiponectin levels. Adiponectin expression increases with PPAR? activation by docosahexanoic acid (DHA). We have previously shown that IUGR results in PPAR? dysregulation in adipose tissue before the onset of obesity and that its expression can be normalized by maternal DHA administration. However, the effect of IUGR and PPAR? activation on adiponectin production in the rat is unknown. We hypothesize that adding DHA to the maternal diet will increase subcutaneous adipose tissue (SAT) adiponectin and adiponectin receptor mRNA and protein and serum adiponectin. IUGR was induced by bilateral uterine artery ligation at E19 of gestation. Maternal rats were fed a standard diet or a 1% DHA diet from E13 to term and during lactation. The effect of IUGR on mRNA levels of adiponectin and its receptors (AdipoR1 and AdipoR2) in SAT and visceral adipose tissue (VAT) of d21 rats was measured by real-time RT-PCR. Serum adiponectin levels were measured by ELISA. Protein levels were measure by western blotting. In regular diet rats, IUGR significantly increased mRNA levels of AdipoR1 in VAT and AdipoR2 in SAT of males. DHA supplementation on IUGR significantly increased mRNA levels of adiponectin (236±16%*), AdipoR1 (189±15%*), and Adipor2 (384± 65%*) in male SAT and adiponectin (199±16%*) and AdipoR2 (425±23%*) in female SAT. AdipoR1and R2 protein levels were increased in male (220±38%; 255±51%*) and female (202±19%*; 229±22%) SAT. Serum adiponectin levels were increased in males (149±13%*) and females (156±11%*). *p