Why the study?
Does ACE2 deficiency worsen epicardial adipose tissue inflammation and cardiac dysfunction in response to diet-induced obesity, and does Ang 1-7 administration reverse this?
Population
ACE2 null and wild-type mice fed a high-fat diet or a control diet, studied at 6 months of age. Also…
Comparison
Ang 1-7 administration and ACE2 knockout vs Wild-type mice, control diet, or ACE2KO-HFD mice…
Design
Preclinical
Follow-up
Studied at 6 months of age
Key result
ACE2 deficiency worsened epicardial adipose tissue inflammation and cardiac dysfunction in response to diet-induced obesity, which was normalized by Ang 1-7 (24 µg/kg/h).
Authors
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May caution against ACE2 inhibition in obese patients; leaves open whether enhancing the ACE2/Ang 1-7 axis improves cardiac outcomes.
Does ACE2 deficiency worsen epicardial adipose tissue inflammation and cardiac dysfunction in response to diet-induced obesity, and does Ang 1-7 administration reverse this?
ACE2 protects against obesity-induced epicardial adipose tissue inflammation and cardiac insulin resistance, suggesting a therapeutic role for the ACE2/Ang 1-7 axis in obesity-related heart failure.
Patel et al. (2015) studied Obesity-mediated cardiac dysfunction. ACE2 deficiency and high-fat diet (with subsequent Ang 1-7 administration) vs. Wild-type mice and control diet was evaluated on Epicardial adipose tissue inflammation and cardiac dysfunction. ACE2 deficiency worsened epicardial adipose tissue inflammation and cardiac dysfunction in response to diet-induced obesity, which was normalized by Ang 1-7 (24 µg/kg/h).