Streptozotocin‐induced type II diabetic rat administered with nonobesogenic high‐fat diet is highly susceptible to myocardial ischemia–reperfusion injury: An insight into the function of mitochondria

Ansari, Mansour; Gopalakrishnan, Senthilkumar; Kurian, Gino A.

doi:10.1002/jcp.27217

Cited by 14 publications

(9 citation statements)

References 39 publications

(48 reference statements)

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“…T2D, Ansari et al. recently reported (in the course of our study) that I–R tolerance is impaired in hearts from rats fed a high‐fat diet for 12 weeks with STZ injection at 8 weeks, yet not from rats subjected to STZ‐dependent hyperglycaemia alone (Ansari, Gopalakrishnan, & Kurian, ), paralleling differing mitochondrial dysfunction. In the db / db genetic model of T2D, Wang et al.…”

Section: Discussionsupporting

confidence: 60%

Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice

Russell

Griffith

Helman

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?What is the impact of chronic adult‐onset diabetes on cardiac ischaemic outcomes and preconditioning? What is the main finding and its importance?Chronic adult‐onset type 2 but not type 1 diabetes significantly impairs myocardial ischaemic tolerance and ischaemic preconditioning. Preconditioning may be detrimental in type 2 diabetes, exaggerating nitrosative stress and apoptotic protein expression. Abstract Effects of diabetes on myocardial responses to ischaemia–reperfusion (I–R) and cardioprotective stimuli remain contentious, potentially reflecting influences of disease duration and time of onset. Chronic adult‐onset type 1 diabetes (T1D) and type 2 diabetes (T2D) were modelled non‐genetically in male C57Bl/6 mice via 5 × 50 mg kg−1 daily streptozotocin (STZ) injections + 12 weeks’ standard chow or 1 × 75 mg kg−1 STZ injection + 12 weeks’ obesogenic diet (32% calories as fat, 57% carbohydrate, 11% protein), respectively. Systemic outcomes were assessed and myocardial responses to I–R ± ischaemic preconditioning (IPC; 3 × 5 min I–R) determined in Langendorff perfused hearts. Uncontrolled T1D was characterised by pronounced hyperglycaemia (25 mm fasting glucose), glucose intolerance and ∼10% body weight loss, whereas T2D mice exhibited moderate hyperglycaemia (15 mm), hyperinsulinaemia, glucose intolerance and 17% weight gain. Circulating ghrelin, resistin and noradrenaline were unchanged with T1D, while leptin increased and noradrenaline declined in T2D mice. Ischaemic tolerance and IPC were preserved in T1D hearts. In contrast, T2D worsened post‐ischaemic function (∼40% greater diastolic and contractile dysfunction) and cell death (100% higher troponin efflux), and abolished IPC protection. Whereas IPC reduced post‐ischaemic nitrotyrosine and pro‐apoptotic Bak and Bax levels in non‐diabetic hearts, these effects were reduced in T1D and IPC augmented Bax and nitrosylation in T2D hearts. The data demonstrate chronic T1D does not inhibit myocardial I–R tolerance or IPC, whereas metabolic and endocrine disruption in T2D is associated with ischaemic intolerance and inhibition of IPC. Indeed, normally protective IPC may exaggerate damage mechanisms in T2D hearts.

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Section: Discussionsupporting

confidence: 60%

Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice

Russell

Griffith

Helman

et al. 2019

Experimental Physiology

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“…Various factors associated with diabetes mellitus, such as impaired calcium homeostasis, altered free fatty acid metabolism, an unbalanced redox state, and increased advanced glycation end products, contribute to cardiovascular complications (Riehle and Bauersachs, 2018;Zhang et al, 2018;Zheng et al, 2018). On the other hand, hypoperfusion of the liver and pancreas, treatment with β-blockers and diuretics, and dysfunction of the autonomic nervous system due to heart failure can impair glucose metabolism (Ansari et al, 2019b). During anti-diabetic drug discovery, targeting common molecules between diabetes mellitus and cardiovascular diseases [such as peroxisome proliferator-activated receptors (PPARs), which are involved in insulin resistance, glucose and lipid metabolism, and systolic or diastolic activity of the left ventricle] may provide a solution to these reciprocal complications (Wu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

et al. 2021

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Matrine, an active component of Sophora flavescens Ait root extracts, has been used in China for years to treat cancer and viral hepatitis. In the present study, we explored the effects of matrine on hyperglycemia-treated cardiomyocytes. Cardiomyocyte function, oxidative stress, cellular viability, and mitochondrial fusion were assessed through immunofluorescence, quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assays, and RNA interference. Matrine treatment suppressed hyperglycemia-induced oxidative stress in cardiomyocytes by upregulating transcription of nuclear factor erythroid 2-like 2 and heme oxygenase-1. Matrine also improved cardiomyocyte contractile and relaxation function during hyperglycemia, and it reduced hyperglycemia-induced cardiomyocyte death by inhibiting mitochondrial apoptosis. Matrine treatment increased the transcription of mitochondrial fusion-related genes and thus attenuated the proportion of fragmented mitochondria in cardiomyocytes. Inhibiting mitochondrial fusion by knocking down mitofusin 2 (Mfn2) abolished the cardioprotective effects of matrine during hyperglycemia. These results demonstrate that matrine could be an effective drug to alleviate hyperglycemia-induced cardiomyocyte damage by activating Mfn2-induced mitochondrial fusion.

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“…It is believed that diabetic complications, such as diabetic-related cardiac dysfunctions, are directly connected with redox imbalance and oxidative stress [9,[11][12][13][14]. Oxidative stress can be described as the lack of ability of the organism to neutralize free radicals, accompanied by overproduction of the latter.…”

Section: Introductionmentioning

confidence: 99%

Effect of Rosmarinic Acid and Sinapic Acid on Oxidative Stress Parameters in the Cardiac Tissue and Serum of Type 2 Diabetic Female Rats

et al. 2019

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Cardiovascular diseases are one of the most common complications of type 2 diabetes. They are considered the leading cause of death among diabetics. One of the mechanisms underlying diabetic cardiovascular complications is oxidative stress. Many phenolic acids are regarded as antioxidants. The aim of the study was to investigate the effect of rosmarinic acid (RA) and sinapic acid (SA) on oxidative stress parameters in the cardiac tissue and serum of type 2 diabetic female rats. Additionally, the effect of these compounds on glucose homeostasis and lipid profile in the serum was evaluated. Type 2 diabetes was induced with high-fat diet and streptozotocin. RA at the doses of 10 and 50 mg/kg and SA at the doses of 5 and 25 mg/kg were administrated orally for 28 days. Untreated diabetic rats exhibited unfavorable changes in glucose metabolism and lipid profile. Changes in the enzymatic and non-enzymatic markers indicated the onset of oxidative stress in these animals. The results showed that the higher doses of the tested phenolic acids—50 mg/kg of RA and 25 mg/kg of SA—revealed beneficial effects on oxidative stress in the cardiac tissue of diabetic rats.

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Streptozotocin‐induced type II diabetic rat administered with nonobesogenic high‐fat diet is highly susceptible to myocardial ischemia–reperfusion injury: An insight into the function of mitochondria

Abstract: The above results suggest that mitochondrial changes associated with diabetes and cardiomyopathy significantly contribute to the adverse outcome of I/R injury.

Cited by 14 publications

References 39 publications

Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice

Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

Effect of Rosmarinic Acid and Sinapic Acid on Oxidative Stress Parameters in the Cardiac Tissue and Serum of Type 2 Diabetic Female Rats

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