Involvement of protein kinase a (PKA) in decreased phosphorylation of phospholamban miocardial induced by obesity

Abstract

Obesity is defined as an excessive or abnormal accumulation of fatty tissue that can deteriorate the health. Experimental researchers have shown that obesity induced by high-fat diet impairs the cardiac function. However, the mechanisms responsible for this dysfunction remain poorly studied. Interstitial fibrosis, myocyte loss and changes in the composition of myosin in intracellular calcium homeostasis and (3-adrenergic system have been suggested as possible responsible for cardiac abnormalities. The (3-adrenergic system plays an important role in the modulation of cardiac performance. Under the action of an agonist such as isoproterenol, the (3-adrenergic receptor, via G protein, adenylate cyclase and cyclic adenosine monophosphate (cAMP), activates protein kinase A (PKA), triggering profound changes in the cycle of intracellular calcium. Studies have reported that PKA regulates cardiac function, metabolic processes, gene expression, cell growth and transport of ions in the heart. Because of our work have observed a reduction of phosphorylation of phospholamban (PLB) at serine 16 in the myocardium in obese rats, and how PKA is responsible for phosphorylating PLB, the purpose of this study will investigate the relationship between PLB and PKA myocardial. Our hypothesis is that the decrease in phosphorylated PLB in obese rats is due to lower expression of PKA myocardial. (AU)