ArticleMolecular and cellular biochemistry2004
Diabetic cardiomyocyte dysfunction and myocyte insulin resistance: role of glucose-induced PKC activity.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 76 citations in OpenAlex.
- Induction on Insulin Resistance In Vitro.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Effects of the angiotensin-converting enzyme inhibitor captopril on occlusal-disharmony-induced cardiac dysfunction in mice.Scientific reports · 2023Article
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- Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022Review
- STIM1-Orai1 interaction mediated calcium influx activation contributes to cardiac contractility of insulin-resistant rats.BMC cardiovascular disorders · 2022Article
- Salvianolic acid A regulates pyroptosis of endothelial cellsFrontiers in pharmacology · 2022Article
- Effects of Puerarin on the Prevention and Treatment of Cardiovascular Diseases.Frontiers in pharmacology · 2021Review
- The Role of BPIFB4 in Immune System and Cardiovascular Disease: The Lesson from Centenarians.Translational medicine @ UniSa · 2021Article
- Stress hyperglycemia, cardiac glucotoxicity, and critically ill patient outcomes current clinical and pathophysiological evidence.Physiological reports · 2021Review
- The Peroxisome Proliferator-Activated Receptor-Gamma Coactivator-1α-Heme Oxygenase 1 Axis, a Powerful Antioxidative Pathway with Potential to Attenuate Diabetic Cardiomyopathy.Antioxidants & redox signaling · 2020Review
- Basic Mechanisms of Diabetic Heart Disease.Circulation research · 2020Review
- Escitalopram Ameliorates Cardiomyopathy in Type 2 Diabetic Rats via Modulation of Receptor for Advanced Glycation End Products and Its Downstream Signaling Cascades.Frontiers in pharmacology · 2020Article
- Diabetic Cardiomyopathy: Current and Future Therapies. Beyond Glycemic Control.Frontiers in physiology · 2018Review
- Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Protein kinase C-mediated sodium glucose transporter 1 activation in precondition-induced cardioprotection.Drug design, development and therapy · 2016Article
- Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.Circulation · 2015Review
- Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes.Circulation research · 2013Review
- Cardiac actions of protein kinase C isoforms.Physiology (Bethesda, Md.) · 2012Review
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Increased protein kinase C (PKC) activity has been implicated in the pathogenesis of a number of diabetic complications, and high concentrations of glucose have been shown to increase PKC activity. The present study was designed to examine the role of PKC in diabetes-induced (and glucose-induced) cardiomyocyte dysfunction and insulin resistance (measured by glucose uptake). Adult rat ventricular myocytes were isolated from nondiabetic and type 1 diabetic animals (4-5 days post-streptozotocin treatment), and maintained overnight, with/without the nonspecific PKC inhibitor chelerythrine (CHEL = 1 microM). Myocyte mechanical properties were evaluated using a video edge-detection system. Basal and insulin-stimulated glucose uptake was measured with [3H]-2-deoxyglucose. Blunted insulin-stimulated glucose uptake was apparent in diabetic myocytes, and both mechanical dysfunctions (e.g., slowed shortening/relengthening) and insulin resistance were maintained in culture, and normalized by CHEL. Cardiomyocytes isolated from nondiabetic animals were cultured in a high concentration of glucose (HG = 25.5 mM) medium, with/without CHEL. HG myocytes exhibited slowed shortening/relengthening and impaired insulin-stimulated glucose uptake compared to myocytes cultured in normal glucose (5.5 mM), and both impairments were prevented by culturing cells in CHEL. Our data support the view that PKC activation contributes to both diabetes-induced abnormal cardiomyocyte mechanics and insulin resistance, and that elevated glucose is sufficient to induce these effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.