ArticleLife sciences2013
Diabetes mellitus reduces the function and expression of ATP-dependent K⁺ channels in cardiac mitochondria.
Article in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Cardioprotective Signaling: Outline and Future Directions.Biomedicines · 2025Review
- Article
- Loss of ATP-sensitive channel expression and function decreases opioid sensitivity in a mouse model of type 2 diabetes.bioRxiv : the preprint server for biology · 2023Article
- Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT-FoxO1 signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Effects of Naringin on Cardiomyocytes From a Rodent Model of Type 2 Diabetes.Frontiers in pharmacology · 2021Article
- Can We Prevent Mitochondrial Dysfunction and Diabetic Cardiomyopathy in Type 1 Diabetes Mellitus? Pathophysiology and Treatment Options.International journal of molecular sciences · 2020Review
- Exploring the mitochondrial microRNA import pathway through Polynucleotide Phosphorylase (PNPase).Journal of molecular and cellular cardiology · 2017Article
- Altered KATP Channel Subunits Expression and Vascular Reactivity in Spontaneously Hypertensive Rats With Age.Journal of cardiovascular pharmacology · 2016Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Triptolide improves systolic function and myocardial energy metabolism of diabetic cardiomyopathy in streptozotocin-induced diabetic rats.BMC cardiovascular disorders · 2015Article
- Cardiac contractile function and mitochondrial respiration in diabetes-related mouse models.Cardiovascular diabetology · 2014Article
- Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies.American journal of physiology. Heart and circulatory physiology · 2014Review
- Gating behavior of endoplasmic reticulum potassium channels of rat hepatocytes in diabetes.Iranian biomedical journal · 2014Article
- Conundrum of pathogenesis of diabetic cardiomyopathy: role of vascular endothelial dysfunction, reactive oxygen species, and mitochondria.Molecular and cellular biochemistry · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
aimOur goal was to determine the effects of type I diabetes mellitus on the function and expression of ATP-dependent K(+) channels in cardiac mitochondria (mitoKATP), composed of a pore-forming subunit (Kir6.1) and a diazoxide-sensitive sulphonylurea receptor (SUR1). We tested the hypothesis that diabetes reduces Kir6.1 and SUR1 expression as well as diazoxide-induced depolarization of mitochondrial membrane potential (ΔΨm). MAIN
methodsMale FVB mice were made diabetic for 5weeks with multiple low dose injections of streptozotocin. Cardiac mitochondria were separated into two populations: subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM). mitoKATP expression was determined via Western blot analysis of Kir6.1 and SUR1 proteins. mitoKATP function was determined by measuring ΔΨm with the potentiometric dye rhodamine 123. KEY
findingsDiabetes reduced Kir6.1 and SUR1 expression in IFM by over 40% (p<0.05 for both). Similarly, diabetes reduced Kir6.1 expression in SSM by approximately 40% (p<0.05); however, SUR1 expression was unaffected. Opening mitoKATP with diazoxide (100μM) depolarized control IFM ΔΨm by 80% of the valinomycin maximum; diabetic IFM depolarized only 30% (p<0.05). Diazoxide-induced depolarization was much less in SSM (20-30%) and unaffected by diabetes. SIGNIFICANCE: Our data indicate that diabetes reduces mitoKATP expression and function in IFM. These changes in mitoKATP may provide an opportunity to understand mechanisms leading to diabetic cardiomyopathy and loss of cardioprotective mechanisms in the diabetic heart.
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