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Distinct transcriptional regulation of long-chain acyl-CoA synthetase isoforms and cytosolic thioesterase 1 in the rodent heart by fatty acids and insulin.

Authors: Durgan, DJ  Smith, JK  Hotze, MA  Egbejimi, O  Cuthbert, KD  Zaha, VG  Dyck, JR  Abel, ED  Young, ME 
Citation: Durgan DJ, etal., Am J Physiol Heart Circ Physiol. 2006 Jun;290(6):H2480-97. Epub 2006 Jan 20.
Pubmed: (View Article at PubMed) PMID:16428347
DOI: Full-text: DOI:10.1152/ajpheart.01344.2005

The molecular mechanism(s) responsible for channeling long-chain fatty acids (LCFAs) into oxidative versus nonoxidative pathways is (are) poorly understood in the heart. Intracellular LCFAs are converted to long-chain fatty acyl-CoAs (LCFA-CoAs) by a family of long-chain acyl-CoA synthetases (ACSLs). Cytosolic thioesterase 1 (CTE1) hydrolyzes cytosolic LCFA-CoAs to LCFAs, generating a potential futile cycle at the expense of ATP utilization. We hypothesized that ACSL isoforms and CTE1 are differentially regulated in the heart during physiological and pathophysiological conditions. Using quantitative RT-PCR, we report that the five known acsl isoforms (acsl1, acsl3, acsl4, acsl5, and acsl6) and cte1 are expressed in whole rat and mouse hearts, as well as adult rat cardiomyocytes (ARCs). Streptozotocin-induced insulin-dependent diabetes (4 wk) and fasting (

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CRRD Object Information
CRRD ID: 1599808
Created: 2007-02-15
Species: All species
Last Modified: 2007-02-15
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.