Altered [3H]ouabain binding to cardiac muscle in insulin‐dependent and non‐insulin‐dependent diabetic rats

Bányász, Tamás; Kovács, Tibor

doi:10.1113/expphysiol.1998.sp004092

Cited by 9 publications

(9 citation statements)

References 35 publications

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“…It is known that reductions in HR are routinely associated with cardiac depression. However, studies undertaking functional comparison at comparable heart rates via pacing in STZ-diabetic rats have reported similar alterations in myocardial contractility despite correcting for HR (41,42). Therefore, the hemodynamic assessment of untreated STZ-diabetic rats in the present study demonstrates that the cardiomyopathy of this pathophysiological condition is characterized by myocardial contractile dysfunction.…”

Section: Discussionsupporting

confidence: 51%

Dietary Supplementation With Vitamin E Ameliorates Cardiac Failure in Type I Diabetic Cardiomyopathy by Suppressing Myocardial Generation of 8-iso-Prostaglandin F2α and Oxidized Glutathione

Hamblin

Smith

Hill

2007

Journal of Cardiac Failure

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Background-Diabetic cardiomyopathy has been documented as an underlying etiology of heart failure (HF) in diabetic patients. Although oxidative stress has been implicated in diabetic cardiomyopathy, much of the current evidence lacks specificity. Furthermore, studies investigating antioxidant protection with vitamin E in this unique cardiac phenomenon have yet to be performed. In the present study, we sought to determine whether vitamin E supplementation can confer cardioprotective effects against diabetic cardiomyopathy in relation to specific and quantitative markers of myocardial oxidative stress.

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Section: Discussionsupporting

confidence: 51%

Dietary Supplementation With Vitamin E Ameliorates Cardiac Failure in Type I Diabetic Cardiomyopathy by Suppressing Myocardial Generation of 8-iso-Prostaglandin F2α and Oxidized Glutathione

Hamblin

Smith

Hill

2007

Journal of Cardiac Failure

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“…Although reductions in heart rate are routinely associated with cardiac depression, studies undertaking functional comparison at comparable heart rates via pacing in STZ-diabetic rats have reported similar alterations in myocardial contractility despite correcting for heart rate [38,39]. Therefore, the LV systolic dysfunction observed in the DM and DM + MI groups cannot merely be the result of the much reduced heart rate and instead points to greater impairment of myocardial contractile function.…”

Section: Discussionmentioning

confidence: 99%

Type 1 diabetes mellitus abrogates compensatory augmentation of myocardial neuregulin-1β/ErbB in response to myocardial infarction resulting in worsening heart failure

Odiete

Konik

Sawyer

et al. 2013

Cardiovasc Diabetol

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BackgroundDiabetes mellitus (DM) patients surviving myocardial infarction (MI) exhibit a substantially higher incidence of subsequent heart failure (HF). Neuregulin (NRG)-1 and erythroblastic leukemia viral oncogene homolog (ErbB) receptors have been shown to play a critical role in maintenance of cardiac function. However, whether myocardial NRG-1/ErbB is altered during post-MI HF associated with DM remains unknown. The aim of this study was to determine the impact of type 1 DM on the myocardial NRG-1/ErbB system following MI in relation to residual left ventricular (LV) function.MethodsType 1 DM was induced in rats via administration of streptozotocin (65 mg/kg, i.p.). Control rats were injected with citrate buffer (vehicle) only. Two weeks after induction of type 1 DM, MI was produced in DM and non-DM rats by ligation of the left coronary artery. Sham MI rats underwent the same surgical procedure with the exception that the left coronary artery was not ligated. At 4 weeks after surgery, residual in vivo LV function was assessed via echocardiography. Myocardial protein expression of NRG-1β, ErbB2 and ErbB4 receptors, and MDM2 (a downstream signaling pathway induced by NRG-1 that has been implicated in cell survival) was assessed in the remaining, viable LV myocardium by Western blotting. Changes in ErbB receptor localization in the surviving LV myocardium of diabetic and non-diabetic post-MI rats was determined using immunohistochemistry techniques.ResultsAt 4 weeks post-MI, echocardiography revealed that LV fractional shortening (FS) and LV ejection fraction (EF) were significantly lower in the DM + MI group compared to the MI group (LVFS: 17.9 ± 0.7 vs. 25.2 ± 2.2; LVEF: 35.5 ± 1.4 vs. 47.5 ± 3.5, respectively; P < 0.05), indicating an increased functional severity of HF among the DM + MI rats. Up-regulation of NRG-1β and ErbB2 protein expression in the MI group was abrogated in the DM + MI group concurrent with degradation of MDM2, a downstream negative regulator of p53. ErbB2 and ErbB4 receptors re-localized to cardiac myocyte nuclei in failing type 1 diabetic post-MI hearts.ConclusionsType 1 DM prevents compensatory up-regulation of myocardial NRG-1/ErbB after MI coincident with an increased severity of HF.

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“…Another explanation is the impairment of Na + /K + -ATPase, a cation membrane transporter. There are reports of altered Na + /K + -ATPase function in myocardial cells of noninsulin-dependent and insulin-dependent DM [46], in cerebral cortex [47] and in peripheral nerves [48] of STZ diabetes-induced adult rats. We found approximately 4-5 mV of depolarization in hyperglycemic animals, and this value is compatible with Na + /K + -ATPase contribution to neuron resting membrane potential [40].…”

Section: Discussionmentioning

confidence: 99%

n5-STZ Diabetic Model Develops Alterations in Sciatic Nerve and Dorsal Root Ganglia Neurons of Wistar Rats

et al. 2013

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One experimental model of diabetes mellitus (DM) similar to type II DM, called n5-STZ, is obtained by a single injection (via i.p.) of streptozotocin (STZ) in the 5th day of life of newborn rats. The present investigation aimed to characterize alterations in excitability of rat peripheral neurons in n5-STZ model. n5-STZ DM was induced, and electrophysiological evaluation was done at 12th week of rat life. Rats developed glucose intolerance, sensory alteration, and hyperglycemia or near-normoglycemia (21.2 ± 1.6 and 7.4 ± 0.4 mmol/L). In near-normoglycemia group the significant electrophysiological alteration observed was decreased in amplitude of 2nd wave (2nd component, conduction velocity: 48.8 m/s) of compound action potential (CAP) of sciatic nerve. For hyperglycemic rats, decreased excitability, amplitude, and conduction velocity of 2nd CAP component of sciatic nerve were found; a depolarization of resting potential (4-5 mV) and reduction in maximum ascendant and descendant inclinations of action potential were found in DRG neurons but no alteration on Na+ current (INa+). Thus, n5-STZ rats develop alterations in excitability which were related to glycemic levels but were not likely attributable to changes on INa+. Our data confirm that n5-STZ model is a useful model to study type II DM.

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Altered [3H]ouabain binding to cardiac muscle in insulin‐dependent and non‐insulin‐dependent diabetic rats

Cited by 9 publications

References 35 publications

Dietary Supplementation With Vitamin E Ameliorates Cardiac Failure in Type I Diabetic Cardiomyopathy by Suppressing Myocardial Generation of 8-iso-Prostaglandin F2α and Oxidized Glutathione

Dietary Supplementation With Vitamin E Ameliorates Cardiac Failure in Type I Diabetic Cardiomyopathy by Suppressing Myocardial Generation of 8-iso-Prostaglandin F2α and Oxidized Glutathione

Type 1 diabetes mellitus abrogates compensatory augmentation of myocardial neuregulin-1β/ErbB in response to myocardial infarction resulting in worsening heart failure

n5-STZ Diabetic Model Develops Alterations in Sciatic Nerve and Dorsal Root Ganglia Neurons of Wistar Rats

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