ArticleMolecular and cellular biochemistry1998
Cardiac sarcolemmal Na(+)-Ca2+ exchange and Na(+)-K+ ATPase activities and gene expression in alloxan-induced diabetes in rats.
Article in Molecular and cellular biochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 49 citations in OpenAlex.
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Cardioprotective effects of naringin in a type 2 diabetes rodent model by reducing calcium overload and oxidative stress.Frontiers in pharmacology · 2025Article
- The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023Review
- Calcium Homeostasis in Ventricular Myocytes of Diabetic Cardiomyopathy.Journal of diabetes research · 2020Review
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Streptozotocin-induced diabetes prolongs twitch duration without affecting the energetics of isolated ventricular trabeculae.Cardiovascular diabetology · 2014Article
- Mechanisms of subcellular remodeling in heart failure due to diabetes.Heart failure reviews · 2014Review
- Alterations in sarcoplasmic reticulum and mitochondrial functions in diabetic cardiomyopathy.Experimental and clinical cardiology · 2012Article
- Diabetic cardiomyopathy: understanding the molecular and cellular basis to progress in diagnosis and treatment.Heart failure reviews · 2012Review
- The chronic effects of neonatal alloxan-induced diabetes mellitus on ventricular myocyte shortening and cytosolic Ca2+.Molecular and cellular biochemistry · 2011Article
- The case for hypoglycaemia as a proarrhythmic event: basic and clinical evidence.Diabetologia · 2010Review
- Diabetic Cardiomyopathy: Mechanisms and Therapeutic Targets.Drug discovery today. Disease mechanisms · 2010Article
- Diabetic cardiomyopathy.Clinical science (London, England : 1979) · 2009Review
- Insulin effects on cardiac Na+/Ca2+ exchanger activity: role of the cytoplasmic regulatory loop.The Journal of biological chemistry · 2008Article
- Proteomic analysis in diabetic cardiomyopathy using bioinformatics approach.Bioinformatics and biology insights · 2008Article
- Differential changes in cardiac myofibrillar and sarcoplasmic reticular gene expression in alloxan-induced diabetes.Molecular and cellular biochemistry · 1999Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To determine the sequence of alterations in cardiac sarcolemmal (SL) Na(+)-Ca2+ exchange, Na(+)-K+ ATPase and Ca(2+)-transport activities during the development of diabetes, rats were made diabetic by an intravenous injection of 65 mg/kg alloxan. SL membranes were prepared from control and experimental hearts 1-12 weeks after induction of diabetes. A separate group of 4 week diabetic animals were injected with insulin (3 U/day) for an additional 4 weeks. Both Na(+)-K+ ATPase and Ca(2+)-stimulated ATPase activities were depressed as early as 10 days after alloxan administration; Mg2+ ATPase activity was not depressed throughout the experimental periods. Both Na(+)-Ca2+ exchange and ATP-dependent Ca(2+)-uptake activities were depressed in diabetic hearts 2 weeks after diabetes induction. These defects in SL Na(+)-K+ ATPase and Ca-transport activities were normalized upon treatment of diabetic animals with insulin. Northern blot analysis was employed to compare the relative mRNA abundances of alpha 1-subunit of Na(+)-K+ ATPase and Na(+)-Ca2+ exchanger in diabetic ventricular tissue vs. control samples. At 6 weeks after alloxan administration, a significant depression of the Na(+)-K+ ATPase alpha 1-subunit mRNA was noted in diabetic heart. A significant increase in the Na(+)-Ca2+ exchanger mRNA abundance was observed at 3 weeks which returned to control by 5 weeks. The results from the alloxan-rat model of diabetes support the view that SL membrane abnormalities in Na(+)-K+ ATPase, Na+Ca2+ exchange and Ca(2+)-pump activities may lead to the occurrence of intracellular Ca2+ overload during the development of diabetic cardiomyopathy but these defects may not be the consequence of depressed expression of genes specific for those SL proteins.
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9823015W1711630333What OpenQuestion holds
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