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Obesity and insulin resistance are major risk factors for cardiovascular disease including cardiomyopathy. Cardiomyopathy is characterized by the reduced ability of heart muscle cells (cardiomyocytes) to contract and/or relax. Maladaptive changes in cardiomyocyte lipid signalling and energy metabolism (increased fatty acid utilization) have been implicated in obesity-induced cardiomyopathy, but the underlying molecular mechanisms are incompletely understood. Lysophosphatidic acid (LPA) has emerged as critical extracellular signalling messenger in the heart that reduces contractility, increases fatty acid delivery, and stimulates hypertrophic remodelling. A major proportion (~40%) of plasma LPA is produced by autotaxin (ATX) secreted from adipose tissue. ATX is a lysophospholipase D that converts lysophosphatidylcholine into LPA in an endocrine or paracrine manner. Interestingly, ATX expression is increased during adipocyte differentiation and in adipose tissue from obese, insulin resistant mice and humans, suggesting that ATX may influence obesity-induced cardiomyopathy. The aim of this research is to examine whether increased circulating LPA due to adipose tissue ATX upregulation following obesity and insulin resistance alters cardiomyocyte energy metabolism and insulin signalling to induce cardiomyopathy.
Biochemistry / Molecular biology
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