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This Article Full Text Full Text (PDF) All Versions of this Article: JME-09-0064v1 43/6/241    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Gutgesell, A. Articles by Eder, K. PubMed PubMed Citation Articles by Gutgesell, A. Articles by Eder, K.

Institute of Agricultural and Nutritional Sciences, Martin-Luther-Universität Halle-Wittenberg, Von-Danckelmann-Platz 2, D-06120 Halle (Saale), Germany
¹ Chair of Animal Nutrition, Center of Life and Food Sciences Weihenstephan, Technische Universität München, Hochfeldweg 1, D-85350 Freising, Germany

(Correspondence should be addressed to K Eder; Email: k.eder{at}wzw.tum.de)

Previous studies have shown that genes involved in fatty acid uptake, fatty acid oxidation, and thermogenesis are downregulated in liver and skeletal muscle of rats during lactation. However, biochemical mechanisms underlying these important metabolic adaptations during lactation have not yet been elucidated. As all these genes are transcriptionally regulated by peroxisome proliferator-activated receptor (Ppar), we hypothesized that their downregulation is mediated by a suppression of Ppar during lactation. In order to investigate this hypothesis, we performed an experiment with lactating and nonlactating Ppar knockout and corresponding wild-type mice. In wild-type mice, lactation led to a considerable downregulation of Ppar, Ppar coactivators Pgc1 and Pgc1β, and Ppar target genes involved in fatty acid uptake, fatty acid oxidation, and thermogenesis in liver and skeletal muscle (P<0.05). Ppar knockout mice had generally a lower expression of all these Ppar target genes in liver and skeletal muscle. However, in those mice, lactation did not lower the expression of genes involved in fatty acid utilization and thermogenesis in liver and skeletal muscle. Expression levels of Ppar target genes in lactating wild-type mice were similar than in lactating or nonlactating Ppar knockout mice. In conclusion, the present findings suggest that downregulation of Ppar and its coactivators in tissues with high rates of fatty acid catabolism is responsible for the reduced utilization of fatty acids in liver and skeletal muscle and the reduced thermogenesis occurring in the lactating animal, which aim to conserve energy and metabolic substrates for milk production in the mammary gland.