ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Upregulation of eNOS and unchanged energy metabolism in increased susceptibility of the aging type 2 diabetic GK rat heart to ischemic injury.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 36 citations in OpenAlex.
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- Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022Review
- Sex Differences of the Diabetic Heart.Frontiers in physiology · 2021Review
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- Voltage dependence of the CaMolecular and cellular biochemistry · 2018Article
- The Impact of Type 2 Diabetes Mellitus on Long-Term Prognosis in Patients of Different Ages with Myocardial Infarction.Journal of diabetes research · 2018Article
- Calcium Signaling in the Ventricular Myocardium of the Goto-Kakizaki Type 2 Diabetic Rat.Journal of diabetes research · 2018Review
- Effects of hypoglycemia on myocardial susceptibility to ischemia-reperfusion injury and preconditioning in hearts from rats with and without type 2 diabetes.Cardiovascular diabetology · 2017Article
- Metabolic Remodeling in Diabetic Cardiomyopathy.Cardiovascular research · 2017Article
- Sex Differences in Metabolic Cardiomyopathy.Cardiovascular research · 2017Article
- Reduced up-regulation of the nitric oxide pathway and impaired endothelial and smooth muscle functions in the female type 2 diabetic goto-kakizaki rat heart.Nutrition & metabolism · 2017Article
- Tissue-specific up-regulation of arginase I and II induced by p38 MAPK mediates endothelial dysfunction in type 1 diabetes mellitus.British journal of pharmacology · 2015Article
- Cardiac NO signalling in the metabolic syndrome.British journal of pharmacology · 2015Review
- Mild Type 2 Diabetes Mellitus Reduces the Susceptibility of the Heart to Ischemia/Reperfusion Injury: Identification of Underlying Gene Expression Changes.Journal of diabetes research · 2015Article
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- Obesity improves myocardial ischaemic tolerance and RISK signalling in insulin-insensitive rats.Disease models & mechanisms · 2013Article
- Arginase: the emerging therapeutic target for vascular oxidative stress and inflammation.Frontiers in immunology · 2013Article
- Perspectives of Targeting mTORC1-S6K1 in Cardiovascular Aging.Frontiers in physiology · 2012Article
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8 authors at 4 institutions in 3 countries.
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Abstract
We investigated the tolerance of the insulin-resistant diabetic heart to ischemic injury in the male Goto-Kakizaki (GK) rat, a model of type 2 diabetes. Changes in energy metabolism, nitric oxide (NO) pathway, and cardiac function were assessed in the presence of physiological substrates. Age-matched control Wistar (n = 19) and GK (n = 18) isolated rat hearts were perfused with 0.4 mM palmitate, 3% albumin, 11 mM glucose, 3 U/l insulin, 0.2 mM pyruvate, and 0.8 mM lactate for 24 min before switching to 1.2 mM palmitate (11 rats/group) during 32 min low-flow (0.5 ml·min(-1)·g wet wt(-1)) ischemia. Next, flow was restored with 0.4 mM palmitate buffer for 32 min. A subset of hearts from each group (n = 8 for control and n = 7 for GK groups) were freeze-clamped for determining baseline values after the initial perfusion of 24 min. ATP, phosphocreatine (PCr), and intracellular pH (pH(i)) were followed using (31)P magnetic resonance spectroscopy with simultaneous measurement of contractile function. The NO pathway was determined by nitric oxide synthase (NOS) isoform expression and total nitrate concentration (NOx) in hearts. We found that coronary flow was 26% lower (P < 0.05) during baseline conditions and 61% lower (P < 0.05) during reperfusion in GK vs. control rat hearts. Rate pressure product was lower during reperfusion in GK vs. control rat hearts (P < 0.05). ATP, PCr, and pH(i) during ischemia-reperfusion were similar in both groups. Endothelial NOS expression was increased in GK rat hearts during baseline conditions (P < 0.05). NOx was increased during baseline conditions (P < 0.05) and after reperfusion (P < 0.05) in GK rat hearts. We report increased susceptibility of type 2 diabetic GK rat heart to ischemic injury that is not associated with impaired energy metabolism. Reduced coronary flow, upregulation of eNOS expression, and increased total NOx levels confirm NO pathway modifications in this model, presumably related to increased oxidative stress. Modifications in the NO pathway may play a major role in ischemia-reperfusion injury of the type 2 diabetic GK rat heart.
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