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Submitted on January 28, 2004
Accepted on May 28, 2004
(PGC-1) expression in the liver is partially dissociated from the control of gluconeogenesis and lipid catabolism
Departament de Bioquímica i Biología Molecular, Universitat de Barcelona. Avda Diagonal 645. 08028-Barcelona, Spain.; Laboratory of Metabolism. National Cancer Institute, Bethesda MD 20892. USA
* To whom correspondence should be addressed. E-mail: gombau{at}porthos.bio.ub.es.
The developmental regulation of PGC-1
gene expression was studied in mice and compared with marker genes of liver energy metabolism. PGC-1 gene was highly expressed in fetal liver compared with adults and remained high in neonatal liver. The regulation of PGC-1 gene expression in the fetal and early neonatal period was dissociated from that of gluconeogenic genes, i.e. the phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) genes. Only under the effects of starvation was PGC-1 gene expression induced in parallel to PEPCK and G6Pase mRNAs during the perinatal period. Furthermore, the PGC-1 gene was not regulated as part of the developmental program of gene expression associated to the maturation of hepatic gluconeogenesis, as revealed by the impaired PEPCK and G6Pase gene expression but unaltered PGC-1 mRNA levels in C/EBP-null fetus and neonates. The regulation of the PGC-1 gene and that of mitochondrial 3-hydroxy-3-methyl.glutaryl-CoA (HMG-CoA) synthase, acyl-CoA oxidase (ACO) and long chain acyl-Co dehydrogenase (LCAD), marker genes of lipid catabolism, were dissociated in fetuses and neonates. The expression of lipid catabolism genes was down-regulated in fasted neonates whereas PGC-1 was oppositely regulated. The independent regulation of the PGC-1 and lipid catabolism genes was also found in PPAR-null neonates, in which PGC-1 mRNA levels were unaffected while gene expression for HMG-CoA synthase and ACO was impaired. Thus, the regulation of the PGC-1 gene is partially dissociated from the patterns of regulation of hepatic genes encoding enzymes involved in gluconeogenesis and lipid catabolism during fetal ontogeny and in response to the initiation of lactation.
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