Cardiac function and intracellular Ca2+ handling proteins are not impaired by high-saturated-fat diet-induced obesity.

A.F Deus,K Okoshi,C.R Padovani,L.C Tomasi,D.H.S Campos,D.C.T Silva,A.C Cicogna,D.F Vileigas

doi:10.1590/1414-431x20198085

Abstract

Obesity is often associated with changes in cardiac function; however, the mechanisms responsible for functional abnormalities have not yet been fully clarified. Considering the lack of information regarding high-saturated-fat diet-induced obesity, heart function, and the proteins involved in myocardial calcium (Ca2+) handling, the aim of this study was to test the hypothesis that this dietary model of obesity leads to cardiac dysfunction resulting from alterations in the regulatory proteins of intracellular Ca2+ homeostasis. Male Wistar rats were distributed into two groups: control (C, n=18; standard diet) and obese (Ob, n=19; high-saturated-fat diet), which were fed for 33 weeks. Cardiac structure and function were evaluated using echocardiographic and isolated papillary muscle analyses. Myocardial protein expressions of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), PLB serine-16 phosphorylation, PLB threonine-17 phosphorylation, ryanodine receptor, calsequestrin, Na+/Ca2+ exchanger, and L-type Ca2+ channel were assessed by western blot. Obese rats presented 104% increase in the adiposity index (C: 4.5±1.4 vs Ob: 9.2±1.5%) and obesity-related comorbidities compared to control rats. The left atrium diameter (C: 5.0±0.4 vs Ob: 5.5±0.5 mm) and posterior wall shortening velocity (C: 36.7±3.4 vs Ob: 41.8±3.8 mm/s) were higher in the obese group than in the control. The papillary muscle function was similar between the groups at baseline and after inotropic and lusitropic maneuvers. Obesity did not lead to changes in myocardial Ca2+ handling proteins expression. In conclusion, the hypothesis was not confirmed, since the high-saturated-fat diet-induced obese rats did not present cardiac dysfunction or impaired intracellular Ca2+ handling proteins.

Highlights

The incidence and prevalence of obesity has increased worldwide, representing a pandemic and, a public health problem [1]
The calorie consumption was similar in both groups and the food intake was lower in the obese animals, the feed efficiency was higher in the Ob group (Table 1)
The aim of this study was to investigate whether obesity promotes cardiac dysfunction due to changes in the expression of myocardial regulatory proteins of intracellular calcium homeostasis

Summary

Introduction

The incidence and prevalence of obesity has increased worldwide, representing a pandemic and, a public health problem [1]. Excess adiposity is strongly associated with increased mortality risk, reduction in life expectancy, and the development of major risk factors for numerous co-morbidities such as type II diabetes mellitus, hyperlipidemia, and cardiovascular diseases [2,3]. Current experimental studies with diet-induced obesity models focus on the amount of fat used and on the source, resulting in diets with a predominance of saturated or unsaturated fatty acids, since they are substantially associated with different outcomes [4]. Research studies confirm that dietary saturated fatty acids are positively associated with increased ventricular remodeling, cardiac hypertrophy, and mitochondrial and contractile dysfunction [5,6,7,8]. Many factors have been presented as responsible for the cardiac changes in obesity, including intracellular calcium (Ca2+) handling [9,10,11,12]. The intracellular Ca2+-cycling proteins located in the sarcolemma and sarcoplasmic reticulum (SR), such as the L-type Ca2+ channel, SR Ca2+-

Objectives

Methods

Results

Conclusion