Transgenic expression of CD36 in the spontaneously hypertensive rat is associated with amelioration of metabolic disturbances but has no effect on hypertension
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.
Grant support
P01 HL35018
NHLBI NIH HHS - United States
R01 HL56028
NHLBI NIH HHS - United States
R01 HL63709
NHLBI NIH HHS - United States
R03 TW01236
FIC NIH HHS - United States
PubMed
14640889
Knihovny.cz E-resources
- MeSH
- CD36 Antigens genetics physiology MeSH
- Diaphragm drug effects metabolism MeSH
- Time Factors MeSH
- Peptide Elongation Factor 1 genetics MeSH
- Epididymis drug effects metabolism MeSH
- Gene Expression MeSH
- Fructose administration & dosage MeSH
- Animals, Genetically Modified MeSH
- Glucose metabolism MeSH
- Glucose Tolerance Test MeSH
- Hyperlipidemias genetics metabolism MeSH
- Hypertension genetics physiopathology MeSH
- Insulin pharmacology MeSH
- Insulin Resistance genetics physiology MeSH
- Liver metabolism MeSH
- Blood Pressure genetics physiology MeSH
- Rats MeSH
- Fatty Acids, Nonesterified blood metabolism MeSH
- Kidney metabolism MeSH
- Lipid Metabolism MeSH
- Myocardium metabolism MeSH
- Area Under Curve MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Rats, Inbred SHR MeSH
- Rats, Wistar MeSH
- Muscles drug effects metabolism MeSH
- Adipose Tissue 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
- Research Support, U.S. Gov't, P.H.S. MeSH
- Names of Substances
- CD36 Antigens MeSH
- Peptide Elongation Factor 1 MeSH
- Fructose MeSH
- Glucose MeSH
- Insulin MeSH
- Fatty Acids, Nonesterified MeSH
Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1 alpha promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure.
Ovariectomy-Induced Hepatic Lipid and Cytochrome P450 Dysmetabolism Precedes Serum Dyslipidemia
