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Increased Maternal Nutrition Stimulates Peroxisome Proliferator Activated Receptor-, Adiponectin, and Leptin Messenger Ribonucleic Acid Expression in Adipose Tissue before Birth

Early Origins of Adult Health Research Group (B.S.M., I.C.M.), The Sansom Research Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide 5000, South Australia, Australia; and the School of Molecular and Biomedical Science (B.S.M., J.A.D., I.C.M.), The University of Adelaide, Adelaide 5005, South Australia, Australia

Address all correspondence and requests for reprints to: Professor I. C. McMillen, Sansom Research Institute, University of South Australia, Adelaide 5000, South Australia, Australia. E-mail: Caroline.McMillen{at}unisa.edu.au.

During fetal life, adipose tissue is predominantly comprised of brown or thermogenic adipocytes and there is a transition to white, lipid-storing adipocytes after birth concomitant with the onset of suckling. In pregnancies complicated by gestational diabetes, the fetus is hyperglycemic, has an increased fat mass, and is at increased risk of obesity in later life. In the present study, we have investigated the hypothesis that exposure to increased maternal nutrition during late gestation results in increased expression of genes that regulate adipogenesis and lipogenesis in perirenal fat in fetal sheep. Pregnant ewes were fed either at or approximately 55% above maintenance energy requirements during late pregnancy and quantitative RT-PCR was used to measure peroxisome proliferator-activated receptor , lipoprotein lipase, glycerol-3-phosphate dehydrogenase, adiponectin, and leptin mRNA expression. We report that exposure to metabolic and hormonal signals of increased nutrition before birth results in an increase in the expression of the adipogenic factor, peroxisome proliferator-activated receptor , and in lipoprotein lipase, adiponectin, and leptin mRNA expression in fetal perirenal fat. We propose that an increase in maternal, and hence fetal, nutrition results in a precocial increase in adipogenic, lipogenic, and adipokine gene expression in adipose tissue and that these changes may be important in the development of obesity in later life.

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