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      Hypoxia in vivo decreases peroxisome proliferator-activated receptor alpha-regulated gene expression in rat heart.

      Biochemical and Biophysical Research Communications

      Anoxia, Carboxy-Lyases, metabolism, Carnitine O-Palmitoyltransferase, Cobalt, pharmacology, Down-Regulation, Energy Metabolism, Gene Expression, drug effects, Heart, physiology, Hemodilution, Isoenzymes, Male, Myocardium, Oxygen, Protein Kinases, Rats, Rats, Sprague-Dawley, Receptors, Cytoplasmic and Nuclear, Transcription Factors, Animals

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          We tested the hypothesis that hypoxia decreases PPARalpha-regulated gene expression in heart muscle in vivo. In two rat models of systemic hypoxia (cobalt chloride treatment and iso-volemic hemodilution), transcript levels of PPARalpha and PPARalpha-regulated genes (pyruvate dehydrogenase kinase 4 (PDK4), muscle carnitine palmitoyltransferase-I (mCPT-I), and malonyl-CoA decarboxylase (MCD)) were measured using real-time quantitative RT-PCR. Data were normalized to the housekeeping gene beta-actin. Atrial natriuretic factor (ANF) and pyruvate dehydrogenase kinase 2 (PDK2), which are not regulated by PPARalpha, served as controls. CoCl(2) treatment decreased PPARalpha, PDK4, mCPT-I, and MCD mRNA levels. Iso-volemic anemia also caused a significant decrease in PPARalpha, PDK4, and MCD mRNA levels. Transcript levels of mCPT-I showed a slight, but not significant decrease (P = 0.08). Gene expression of beta-actin, ANF, and PDK2 did not change with either CoCl(2) treatment nor with anemia. Myocardial PPARalpha-regulated gene expression is decreased in two models of hypoxia in vivo. These results suggest a transcriptional mechanism for decreased fatty oxidation and increased reliance of the heart for glucose during hypoxia. Copyright 2001 Academic Press.

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