Key result
Streptozotocin-induced diabetes significantly increased the amplitude of Ca2+ transients and decreased the Na+/Ca2+ exchanger current in epicardial and endocardial ventricular myocytes.
Why the study?
Abnormalities in Ca2+ signaling have a key role in hemodynamic dysfunction in the diabetic heart, but the regional effects of diabetes on epicardial and endocardial left ventricular myocytes required exploration.
Does streptozotocin-induced diabetes alter calcium signaling and Na+/Ca2+ exchanger function in epicardial and endocardial ventricular myocytes in a rat model?
Does streptozotocin-induced diabetes alter calcium signaling and Na+/Ca2+ exchanger function in epicardial and endocardial ventricular myocytes in a rat model?
This preclinical study highlights that dysfunction in the Na+/Ca2+ exchanger is a key mechanism behind pathological increases in calcium transients in diabetic cardiomyopathy, offering potential basic science targets for heart failure.
Answers are grounded in this paper and cite their sources.
Implicates NCX dysfunction in diabetic cardiomyopathy; hypothesis-generating and should not yet change practice.
Aims/Introduction Abnormalities in Ca 2+ signaling have a key role in hemodynamic dysfunction in diabetic heart. The purpose of this study was to explore the effects of streptozotocin (STZ)‐induced diabetes on Ca 2+ signaling in epicardial (EPI) and endocardial (ENDO) cells of the left ventricle after 5–6 months of STZ injection. Materials and Methods Whole‐cell patch clamp was used to measure the L‐type Ca 2+ channel (LTCC) and Na + /Ca 2+ exchanger currents. Fluorescence photometry techniques were used to measure intracellular free Ca 2+ concentration. Results Although the LTCC current was not significantly altered, the amplitude of Ca 2+ transients increased significantly in EPI‐STZ and ENDO‐STZ compared with controls. Time to peak LTCC current, time to peak Ca 2+ transient, time to half decay of LTCC current and time to half decay of Ca 2+ transients were not significantly changed in EPI‐STZ and ENDO‐STZ myocytes compared with controls. The Na + /Ca 2+ exchanger current was significantly smaller in EPI‐STZ and in ENDO‐STZ compared with controls. Conclusions STZ‐induced diabetes resulted in an increase in amplitude of Ca 2+ transients in EPI and ENDO myocytes that was independent of the LTCC current. Such an effect can be attributed, at least in part, to the dysfunction of the Na + /Ca 2+ exchanger. Additional studies are warranted to improve our understanding of the regional impact of diabetes on Ca 2+ signaling, which will facilitate the discovery of new targeted treatments for diabetic cardiomyopathy.
No takes yet. Share an insight, caveat, or question.
Kury et al. (2020) studied Diabetic cardiomyopathy (Streptozotocin-induced diabetes model). Streptozotocin-induced diabetes vs. Age-matched controls injected with citrate buffer alone was evaluated on Amplitude of Ca2+ transients and Na+/Ca2+ exchanger (NCX) current (p=<0.05). Streptozotocin-induced diabetes significantly increased the amplitude of Ca2+ transients and decreased the Na+/Ca2+ exchanger current in epicardial and endocardial ventricular myocytes.
Synapse has enriched 10 related papers. Consider them for comparative context: