Efeito de diferentes doses de hormônios tireoidianos sobre a expressão gênica e protéica de proteínas relacionadas ao trânsito de cálcio em animais obesos e obesos submetidos à restrição alimentar

Abstract

The underlying cause of obesity is multifactorial and is probably a combination of genetic, environmental and psychosocial factors that determine the balance between food intake and energy expenditure. Clinical studies show that obesity is associated with ventricular dysfunction, usually diastolic. The relationship between obesity and transit of intracellular Ca2+ has been studied by molecular biology techniques, which make possible the understanding of the mechanisms responsible for changes in myocardial performance. The transit of intracellular calcium is regulated by Na+ / Ca2+, L channel, sarcoplasmic reticulum (SR), channel ryanodine (RYR2), SR Ca2+ pump ATPase (SERCA2), phospholamban (PLB). Few studies that evaluated the proteins involved in intracellular Ca2+ homeostasis of the myocardium in model experimental showed divergent results in obesity. It is known that obesity and administration of T3 may alter the gene and protein expression of the transit of calcium in the heart. Food restriction is the most common strategy for treating obesity and has a central role in fat reduction in obese subjects. Few studies have examined the molecular mechanisms related to myocardial Ca2+ cycle in the heart of restricted animals. So any change in the expression of Ca2+ related genes could lead to abnormal Ca2+ homeostasis and, consequently, contractile dysfunction in heart tissue of rats restricted. The objective of this study was to analyze the influence of obesity and food restriction on administration of different doses of thyroid hormone on gene and protein expression of proteins related to the transit of cardiac calcium. For this, male Wistar rats were randomized and initially divided into two groups: control (C) and obese (OB). Group C received a standard diet and OB animals... (Complete abstract click electronic access below)