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Am J Physiol Regul Integr Comp Physiol 280: R183-R190, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 1, R183-R190, January 2001

Uteroplacental insufficiency alters hepatic fatty acid-metabolizing enzymes in juvenile and adult rats

Robert H. Lane1, David E. Kelley2, Elisa M. Gruetzmacher2, and Sherin U. Devaskar1

1 Department of Pediatrics, University of California Los Angeles School of Medicine, Mattel Children's Hospital at UCLA, Los Angeles, California 90095; and 2 Departments of Internal Medicine and Pediatrics, University of Pittsburgh School of Medicine, Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15213

Multiple adult morbidities are associated with intrauterine growth retardation (IUGR) including dyslipidemia. We hypothesized that uteroplacental insufficiency and subsequent IUGR in the rat would lead to altered hepatic fatty acid metabolism. To test this hypothesis, we quantified hepatic mRNA levels of acetyl-CoA carboxylase (ACC), carnitine palmitoyltransferase (CPTI), the beta -oxidation-trifunctional protein (HADH), fasting serum triglycerides, and hepatic malonyl-CoA levels at different ages in control and IUGR rats. Fetal gene expression of all three enzymes was decreased. Juvenile gene expression of CPTI and HADH continued to be decreased, whereas gene expression of ACC was increased. Serum triglycerides were unchanged. A sex-specific response was noted in the adult rats. In males, serum triglycerides, hepatic malonyl-CoA levels, and ACC mRNA levels were significantly increased, and CPTI and HADH mRNA levels were significantly decreased. In contrast, the female rats demonstrated no significant changes in these variables. These results suggest that uteroplacental insufficiency leads to altered hepatic fatty acid metabolism that may contribute to the adult dyslipidemia associated with low birth weight.

intrauterine growth retardation; syndrome X; dyslipidemia


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