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Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling
Artur Junio Togneri Ferron1, Bruno Barcellos Jacobsen1, Paula Grippa Sant'Ana2
1Center of Physical Education and Sports, Department of Sports, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Insights
Obesity impairs heart function, but this study found no evidence of beta-adrenergic receptor system dysfunction. The observed myocardial issues in obese rats were not linked to the beta-adrenergic pathway.
Area of Science:
- Cardiology
- Metabolic Disorders
- Molecular Biology
Background:
- Obesity is linked to impaired myocardial performance.
- The beta-adrenergic (βA) system regulates cardiac contraction and relaxation.
- Potential cardiac abnormalities in obesity may involve the βA system.
Purpose of the Study:
- To investigate the role of βA system components in obesity-induced myocardial dysfunction.
- To determine if βA receptor signaling is altered in obesity.
Main Methods:
- Wistar rats were fed standard or high-fat diets for 15 weeks to induce obesity.
- Cardiac function was assessed using isolated papillary muscle preparations.
- βA system function and protein expression (Gsα, β1AR, β2AR) were evaluated.
Main Results:
- Obese rats showed increased adiposity and comorbidities but unchanged systolic blood pressure.
- Obesity led to structural changes and compromised myocardial responsiveness to stimuli and calcium.
- No significant changes in cardiac function were observed after βA stimulation.
- Protein expression of Gsα, β1AR, and β2AR remained unchanged in obese rats.
Conclusions:
- Myocardial dysfunction in diet-induced obesity is not associated with impairment of the βA receptor-signaling pathway after 15 weeks.
- The study suggests other mechanisms contribute to cardiac abnormalities in obesity.
Abstract:
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.
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