Rosiglitazone fails to improve hypertriglyceridemia and glucose tolerance in CD36-deficient BN.SHR4 congenic rat strain
Language English Country United States Media electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
12429866
DOI
10.1152/physiolgenomics.00113.2002
PII: 00113.2002
Knihovny.cz E-resources
- MeSH
- CD36 Antigens genetics physiology MeSH
- Administration, Oral MeSH
- Diet statistics & numerical data MeSH
- Glucose Tolerance Test MeSH
- Hypertriglyceridemia drug therapy genetics metabolism MeSH
- Hypoglycemic Agents administration & dosage pharmacology therapeutic use MeSH
- Insulin agonists physiology MeSH
- Dietary Sucrose metabolism MeSH
- Rats MeSH
- Glucose Intolerance drug therapy genetics metabolism MeSH
- Rats, Inbred BN MeSH
- Rats, Inbred SHR MeSH
- Rosiglitazone MeSH
- Body Composition drug effects genetics MeSH
- Thiazolidinediones * MeSH
- Thiazoles administration & dosage pharmacology therapeutic use MeSH
- Adipose Tissue drug effects metabolism MeSH
- Adipocytes drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- CD36 Antigens MeSH
- Hypoglycemic Agents MeSH
- Insulin MeSH
- Dietary Sucrose MeSH
- Rosiglitazone MeSH
- Thiazolidinediones * MeSH
- Thiazoles MeSH
The favorable metabolic effects of thiazolidinediones are supposedly related to the peroxisome proliferator-activated receptor-gamma (PPARgamma)-driven changes in lipid metabolism, particularly in free fatty acid (FFA) trafficking. The fatty acid translocase CD36 is one of the proposed PPARgamma targets to mediate this action. We assessed the effect of rosiglitazone (RSG, Avandia) administration in two inbred rat strains, BN/Cub and BN.SHR4 congenic strain, differing in 10 cM proximal segment of chromosome 4. Rats were fed high-sucrose diet with or without RSG for 1 wk. In BN.SHR4, which carries defective Cd36 allele of SHR origin, RSG 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 RSG-treated BN.SHR4 showed lower concentrations of FFA and substantial increase in glycogen synthesis and glucose oxidation in skeletal muscle. Altogether, these results support involvement of CD36 in RSG action, suggesting this pharmacogenetic interaction may be of particular importance in CD36-deficient humans.
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