Why the study?
Cardiovascular complications and electromechanical dysfunction are widely reported in the diabetic heart, but the effects of obesity and diabesity on myocyte shortening and Ca2+ signaling required investigation.
Diabesity in Zucker rats prolongs time to peak myocyte shortening and alters Ca2+ transient decay, suggesting defective sarcoplasmic reticulum Ca2+ handling.
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Prolonged TPK shortening in ZDF myocytes signals early electromechanical impairment; leaves open whether Ca2+ handling defects translate to human diabetic cardiomyopathy.
Sultan et al. (2025) studied this question.
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