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Articles in PresS, published online ahead of print November 12, 2002
Physiol Genomics, 10.1152/physiolgenomics.00113.2002
Submitted on September 3, 2002
Accepted on November 6, 2002
1 Institute of Biology and Medical Genetics, First Faculty of Medicine of Charles University, Prague, Czech Republic; Institute for Clinical and Experimental Medicine, Prague, Czech Republic
2 Institute for Clinical and Experimental Medicine, Prague, Czech Republic
3 Institute of Biology and Medical Genetics, First Faculty of Medicine of Charles University, Prague, Czech Republic
4 Institute of Biology and Medical Genetics, First Faculty of Medicine of Charles University, Prague, Czech Republic; Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
* To whom correspondence should be addressed. E-mail: oseda{at}aol.com.
The favorable metabolic effects of thiazolidinediones are supposedly related to the PPAR
driven changes in lipid metabolism, particularly in free fatty acid trafficking. The fatty acid translocase CD36 is one of the proposed PPAR targets to mediate this action. We assessed the effect of rosiglitazone (Avandia) administration in two inbred rat strains, BN/Cub and BN.SHR4 congenic strain, differing in 10cM proximal segment of chromosome 4. Rats were fed high-sucrose diet with or without rosiglitazone for 1 week. In BN.SHR4, which carries defective Cd36 allele of SHR origin, rosiglitazone failed to improve glucose tolerance (assessed by the oral glucose tolerance test), did not lower triglyceridemia nor induced increases in epididymal and retroperitoneal adipose tissue weights and adipose tissue glucose utilization, effects observed in BN/Cub. On the other hand, the rosiglitazone-treated BN.SHR4 showed lower concentrations of free fatty acids and substantial increase in glycogen synthesis and glucose oxidation in skeletal muscle. Altogether, these results support involvement of CD36 in rosiglitazone action, suggesting this pharmacogenetic interaction may be of particular importance in CD36 deficient humans.
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