Obesity has been shown to impair myocardial performance. Some factors have been suggested as responsible for possible cardiac abnormalities in models of obesity, among them beta-adrenergic (βA) system, an important mechanism of regulation of myocardial contraction and relaxation. The objective of present study was to evaluate the involvement of βA system components in myocardial dysfunction induced by obesity. Thirty-day-old male Wistar rats were distributed in control (C, n = 25) and obese (Ob, n = 25) groups. The C group was fed a standard diet and Ob group was fed four unsaturated high-fat diets for 15 weeks. Cardiac function was evaluated by isolated papillary muscle preparation and βA system evaluated by using cumulative concentrations of isoproterenol and Western blot. After 15 weeks, the Ob rats developed higher adiposity index than C rats and several comorbidities; however, were not associated with changes in systolic blood pressure. Obesity caused structural changes and the myocardial responsiveness to post-rest contraction stimulus and increased extracellular calcium (Ca2+) was compromised. There were no changes in cardiac function between groups after βA stimulation. The obesity was not accompanied by changes in protein expression of G protein subunit alpha (Gsα) and βA receptors (β1AR and β2AR). In conclusion, the myocardial dysfunction caused by unsaturated high-fat diet-induced obesity, after 15 weeks, is not related to βAR system impairment at the receptor-signalling pathway.
BackgroundDiet-induced obesity is frequently used to demonstrate cardiac dysfunction.
However, some rats, like humans, are susceptible to developing an obesity
phenotype, whereas others are resistant to that.ObjectiveTo evaluate the association between obesity resistance and cardiac function, and
the impact of obesity resistance on calcium handling.MethodsThirty-day-old male Wistar rats were distributed into two groups, each with 54
animals: control (C; standard diet) and obese (four palatable high-fat diets) for
15 weeks. After the experimental protocol, rats consuming the high-fat diets were
classified according to the adiposity index and subdivided into obesity-prone (OP)
and obesity-resistant (OR). Nutritional profile, comorbidities, and cardiac
remodeling were evaluated. Cardiac function was assessed by papillary muscle
evaluation at baseline and after inotropic maneuvers.ResultsThe high-fat diets promoted increase in body fat and adiposity index in OP rats
compared with C and OR rats. Glucose, lipid, and blood pressure profiles remained
unchanged in OR rats. In addition, the total heart weight and the weight of the
left and right ventricles in OR rats were lower than those in OP rats, but similar
to those in C rats. Baseline cardiac muscle data were similar in all rats, but
myocardial responsiveness to a post-rest contraction stimulus was compromised in
OP and OR rats compared with C rats.ConclusionObesity resistance promoted specific changes in the contraction phase without
changes in the relaxation phase. This mild abnormality may be related to
intracellular Ca2+ handling.
BackgroundDifferent types of high-fat and/or high-energy diets have been used to induce
obesity in rodents. However, few studies have reported on the effects
observed at the initial stage of obesity induced by high-fat feeding on
cardiac functional and structural remodelling.ObjectiveTo characterize the initial moment of obesity and investigate both metabolic
and cardiac parameters. In addition, the role of Ca2+ handling in
short-term exposure to obesity was verified.MethodsThirty-day-old male Wistar rats were randomized into two groups (n = 19
each): control (C; standard diet) and high-fat diet (HF, unsaturated
high-fat diet). The initial moment of obesity was defined by weekly
measurement of body weight (BW) complemented by adiposity index (AI).
Cardiac remodelling was assessed by morphological, histological,
echocardiographic and papillary muscle analysis. Ca2+ handling
proteins were determined by Western Blot.ResultsThe initial moment of obesity occurred at the 3rd week. Compared
with C rats, the HF rats had higher final BW (4%), body fat (20%), AI
(14.5%), insulin levels (39.7%), leptin (62.4%) and low-density lipoprotein
cholesterol (15.5%) but did not exhibit alterations in systolic blood
pressure. Echocardiographic evaluation did not show alterations in cardiac
parameters. In the HF group, muscles were observed to increase their +dT/dt
(C: 52.6 ± 9.0 g/mm2/s and HF: 68.0 ± 17.0
g/mm2/s; p < 0.05). In addition, there was no changes in
the cardiac expression of Ca2+ handling proteins.ConclusionThe initial moment of obesity promotes alterations to hormonal and lipid
profiles without cardiac damage or changes in Ca2+ handling.
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