Key result
Obesity resistance in rats fed a high-fat diet compromised myocardial responsiveness to a post-rest contraction stimulus compared with control rats, without changes in the relaxation phase.
Why the study?
Does obesity resistance prevent cardiac contractile dysfunction in rats fed a high-fat diet?
Does obesity resistance prevent cardiac contractile dysfunction in rats fed a high-fat diet?
Even in the absence of an obesity phenotype, high-fat diet consumption in rats promotes mild cardiac contractile dysfunction associated with intracellular calcium handling.
High-fat diet may impair rat myocardial contractility independent of obesity; leaves open translation to human calcium handling or practice.
BACKGROUND: Diet-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. OBJECTIVE: To evaluate the association between obesity resistance and cardiac function, and the impact of obesity resistance on calcium handling. METHODS: Thirty-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. RESULTS: The 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. CONCLUSION: Obesity resistance promoted specific changes in the contraction phase without changes in the relaxation phase. This mild abnormality may be related to intracellular Ca2+ handling.
No takes yet. Share an insight, caveat, or question.
Sá et al. (2015) studied Obesity and cardiac dysfunction (n=108). High-fat diet (obesity-resistant phenotype) vs. Standard diet (control) and obesity-prone phenotype was evaluated on Cardiac function assessed by papillary muscle evaluation at baseline and after inotropic maneuvers. Obesity resistance in rats fed a high-fat diet compromised myocardial responsiveness to a post-rest contraction stimulus compared with control rats, without changes in the relaxation phase.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: