High-fat diet-induced cardiac contractile dysfunction in rats is linked to CD36 relocation to the sarcolemma, leading to increased fatty acid uptake and lipid accumulation, suggesting a mechanism for diabetic cardiomyopathy.
Supports CD36-mediated lipotoxicity in rodent cardiomyopathy; leaves open human translational relevance.
Feeding rats an HFD induced cardiac contractile dysfunction, which was accompanied by the relocation of CD36 to the sarcolemma, and elevated basal levels of phosphorylated PKB/Akt. The permanent presence of CD36 at the sarcolemma resulted in enhanced rates of LCFA uptake and myocardial triacylglycerol accumulation, and may contribute to the development of insulin resistance and diabetic cardiomyopathy.
No takes yet. Share an insight, caveat, or question.
Ouwens et al. (2007) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: