Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-01

AUTHORS

Timothy J. Aitman, Anne M. Glazier, Caroline A. Wallace, Lisa D. Cooper, Penny J. Norsworthy, Faisal N. Wahid, Khulood M. Al-Majali, Paul M. Trembling, Christopher J. Mann, Carol C. Shoulders, Daniel Graf, Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Michal Pravenec, Azeddine Ibrahimi, Nada A. Abumrad, Lawrence W. Stanton, James Scott

ABSTRACT

The human insulin-resistance syndromes, type 2 diabetes, obesity, combined hyperlipidaemia and essential hypertension, are complex disorders whose genetic basis is unknown. The spontaneously hypertensive rat (SHR) is insulin resistant and a model of these human syndromes. Quantitative trait loci (QTLs) for SHR defects in glucose and fatty acid metabolism, hypertriglyceridaemia and hypertension map to a single locus on rat chromosome 4. Here we combine use of cDNA microarrays, congenic mapping and radiation hybrid (RH) mapping to identify a defective SHR gene, Cd36 (also known as Fat, as it encodes fatty acid translocase), at the peak of linkage to these QTLs. SHR Cd36 cDNA contains multiple sequence variants, caused by unequal genomic recombination of a duplicated ancestral gene. The encoded protein product is undetectable in SHR adipocyte plasma membrane. Transgenic mice overexpressing Cd36 have reduced blood lipids. We conclude that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridaemia in SHR and may be important in the pathogenesis of human insulin-resistance syndromes. More... »

PAGES

76

Journal

TITLE

Nature Genetics

ISSUE

1

VOLUME

21

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/5013

DOI

http://dx.doi.org/10.1038/5013

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1013810551

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9916795


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