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Am J Physiol Endocrinol Metab 291: E420-E427, 2006. First published April 11, 2006; doi:10.1152/ajpendo.00083.2006
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Altered cardiac fatty acid composition and utilization following dexamethasone-induced insulin resistance

Dake Qi,1 Ding An,1 Girish Kewalramani,1 Yadan Qi,1 Thomas Pulinilkunnil,1 Ashraf Abrahani,1 Usama Al-Atar,1 Sanjoy Ghosh,1 Richard B. Wambolt,2 Michael F. Allard,2 Sheila M. Innis,3 and Brian Rodrigues1

1Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, 2Department of Pathology and Laboratory Medicine, and 3Department of Pediatrics, The University of British Columbia, Vancouver, British Columbia, Canada

Submitted 17 February 2006 ; accepted in final form 2 April 2006

Glucocorticoid therapy is often associated with impaired insulin sensitivity and cardiovascular disease. The present study was designed to evaluate cardiac fatty acid (FA) composition and metabolism following acute dexamethasone (Dex) treatment. Using the euglycemic hyperinsulinemic clamp, rats injected with Dex demonstrated a reduced glucose infusion rate. This whole body insulin resistance was also associated with a heart-specific increase in pyruvate dehydrogenase kinase 4 gene expression and a reduction in the rate of glucose oxidation. Dex treatment increased basal and postheparin plasma lipolytic activity. In the heart, palmitic and oleic acid levels were higher after 4 h of Dex and decreased to control (CON) levels within 8 h. Measurement of polyunsaturated FAs demonstrated a drop in linoleic and {gamma}-linolenic acid, with an increase in arachidonic acid (AA) after acute Dex injection. Tissue FA can be either oxidized or stored as triglyceride (TG). At 4 h, Dex augmented cardiac TG accumulation. However, this increase in tissue TG could not be maintained, such that at 8 h following Dex, TG declined to CON levels. AMP-activated protein kinase (AMPK) activation is known to promote FA oxidation through its control of acetyl-CoA carboxylase (ACC). Acute Dex promoted ACC phosphorylation, and increased cardiac palmitate oxidation, likely through its effects in increasing AMPK phosphorylation and total AMPK protein and gene expression. Whether these acute effects of Dex on FA oxidation, TG storage, and arachidonic acid accumulation can be translated into increased cardiovascular risk following chronic therapy has yet to be determined.

palmitate oxidation; adenosine 5'-monophosphate-activated protein kinase; acetyl-coenzyme A carboxylase; lipoprotein lipase; polyunsaturated fatty acid


Address for reprint requests and other correspondence: B. Rodrigues, Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The Univ. of British Columbia, 2146 East Mall, Vancouver, BC, Canada V6T 1Z3 (e-mail: rodrigue{at}interchange.ubc.ca)




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