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Article

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

Nature genetics - 1 Jan 1999

Aitman T J, Glazier A M, Wallace C A, Cooper L D, Norsworthy P J, Wahid F N, Al-Majali K M, Trembling P M, Mann C J, Shoulders C C, Graf D, St Lezin E, Kurtz T W, Kren V, Pravenec M, Ibrahimi A, Abumrad N A, Stanton L W, Scott J

Abstract excerpt

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...

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PMID: 9916795
DOI: 10.1038/5013

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats.PMID 9916795Read ↗

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CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis.Semantic proximity Read ↗

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