Defect in human myocardial long-chain fatty acid uptake is caused by FAT/CD36 mutations.
J Lipid Res
; 42(5): 751-9, 2001 May.
Article
em En
| MEDLINE
| ID: mdl-11352982
ABSTRACT
Because of the importance of long-chain fatty acids (LCFAs) as a myocardial energy substrate, myocardial LCFA metabolism has been of particular interest for the understanding of cardiac pathophysiology. Recently, by using radiolabeled LCFA analogues, myocardial LCFA metabolism has been clinically evaluated, which revealed a total defect of myocardial LCFA accumulation in a small number of subjects. The mechanism for the cellular LCFA uptake process is still disputable, but recent results suggest that fatty acid translocase (FAT)/CD36 is a transporter in the heart. In the present study, we analyzed mutations and protein expression of the FAT/CD36 gene in 47 patients who showed total lack of the accumulation of a radiolabeled LCFA analogue in the heart. All the patients carried two mutations in the FAT/CD36 gene, and expression of the FAT/CD36 protein was not detected on either platelet or monocyte membranes. Our results showed the link between mutations of the FAT/CD36 gene and a defect in the accumulation of LCFAs in the human heart.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Glicoproteínas de Membrana
/
Doenças Cardiovasculares
/
Antígenos CD36
/
Transportadores de Ânions Orgânicos
/
Ácidos Graxos
/
Miocárdio
Tipo de estudo:
Observational_studies
Limite:
Adolescent
/
Adult
/
Aged
/
Aged80
/
Humans
/
Middle aged
Idioma:
En
Revista:
J Lipid Res
Ano de publicação:
2001
Tipo de documento:
Article
País de afiliação:
Japão