Key result
Diabetic epicardial adipose tissue secretions impair cardiomyocyte contractile function and insulin signaling vs controls.
Why the study?
Secreted factors from epicardial adipose tissue in patients with type 2 diabetes mellitus may contribute to cardiomyocyte dysfunction, but the specific alterations and effects were unclear.
Do secretory products from epicardial adipose tissue of patients with type 2 diabetes mellitus induce cardiomyocyte dysfunction?
Population
Primary adult rat cardiomyocytes and EAT biopsies from patients with and without type 2 diabetes mellitus
Comparison
Conditioned media from EAT of DM2 patients versus conditioned media from EAT of non-DM2 patients and from subcutaneous and pericardial adipose tissue
Design
Preclinical study using primary cardiomyocytes incubated with conditioned media from human adipose tissue explants
Authors
Loading...
EAT-derived factors may contribute to diabetic cardiomyopathy; hypothesis-generating for activin A targeting and requires human validation.
Do secretory products from epicardial adipose tissue of patients with type 2 diabetes mellitus induce cardiomyocyte dysfunction?
Secretory products from epicardial adipose tissue in patients with type 2 diabetes, specifically activin A, induce cardiomyocyte dysfunction, implicating EAT in the pathogenesis of diabetes-related heart disease.
Greulich et al. (2012) studied Type 2 diabetes mellitus. Conditioned media from epicardial adipose tissue of patients with DM2 vs. Conditioned media from epicardial adipose tissue of patients without DM2 and other fat depots was evaluated on Cardiomyocyte contractile function and insulin action. Conditioned media from epicardial adipose tissue of patients with type 2 diabetes reduced cardiomyocyte contractile function and insulin action compared with controls.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: