Cardiac Functional Analysis by Electrocardiography, Echocardiography and in situ Hemodynamics in Streptozotocin-Induced Diabetic Mice

Li, Yan; Gu, Yu; Song, Ye; Zhang, Li; Kang, Y. James; Prabhu, Sumanth D.; Cai, Lu

doi:10.1248/jhs.50.356

Cited by 12 publications

(12 citation statements)

References 38 publications

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“…We supplied Zn to diabetic mice for only 3 months after diagnosis of diabetes for the following 2 reasons: (1) Diabetic cardiomyopathy, although a chronic symptom, is believed to be secondary to early cardiac injuries caused by diabetes 22,34,35 ; and (2) we have found that a temporal and recoverable cardiac dysfunction could be observed in diabetic mice at an early stage (Ϸ2 weeks), 13,22 which was also noted in diabetic rats. 36 However, irreversible cardiac dysfunction may begin at Ϸ3 months after streptozotocin treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Zn supplementation for 3 months was selected because we found that diabetic mice 3 months after induction of hyperglycemia started to show cardiac dysfunction by echocardiography and other assessments. 22 Among the nondiabetic mice, 5 Zn-supplemented and 5 non-Znsupplemented mice were euthanized at 1 month and 3 months after Zn supplementation to harvest the heart and liver for measurement of cardiac and hepatic MT contents and hepatic mineral contents.…”

Section: Supplementation With Znmentioning

confidence: 99%

“…22,23 Mice were anesthetized with tribromoethanol (0.5 mg/g body wt, by 0.25 mL/g IP injection). A midline incision (1 to 2 cm) in the throat area external to the trachea was made for the insertion of a PE-100 catheter to ensure a patent airway.…”

Section: Assessment Of Left Ventricular Performancementioning

confidence: 99%

“…14 For MT expression, cardiac sections were stained as described previously. 22 The Sirius red-stained sections were assessed for the proportion of fibrosis (collagen) in the heart tissues by semiquantitative analysis on the basis of a 1 to 4 scoring method, as described previously. 24,25 …”

Section: Histopathological Examination By Light and Electron Microscopymentioning

confidence: 99%

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Cardiac Metallothionein Induction Plays the Major Role in the Prevention of Diabetic Cardiomyopathy by Zinc Supplementation

et al. 2006

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Background-Our previous studies showed that transgenic mice that overexpress cardiac-specific metallothionein (MT) are highly resistant to diabetes-induced cardiomyopathy. Zinc is the major metal that binds to MT under physiological conditions and is a potent inducer of MT. The present study therefore explored whether zinc supplementation can protect against diabetic cardiomyopathy through cardiac MT induction. Methods and Results-Diabetes was induced in mice (C57BL/6J strain) by a single injection of streptozotocin. Half were supplemented intraperitoneally with zinc sulfate (5 mg/kg) every other day for 3 months. After zinc supplementation, mice were maintained for 3 more months and then examined for cardiomyopathy by functional and morphological analysis. Significant increases in cardiac morphological impairment, fibrosis, and dysfunction were observed in diabetic mice but not in diabetic mice supplemented with zinc. Zinc supplementation also induced a significant increase in cardiac MT expression. The role of MT in cardiac protection by zinc supplementation was examined in cultured cardiac cells that were directly exposed to high levels of glucose (HG) and free fatty acid (FFA) (palmitate), treatment that mimics diabetic conditions. Cell survival rate was significantly decreased for cells exposed to HG/FFA but did not change for cells exposed to HG/FFA and pretreated with zinc or low-dose cadmium, each of which induces significant MT synthesis. When MT expression was silenced with the use of MT small-interfering RNA, the preventive effect of pretreatment with zinc or low-dose cadmium was abolished. Conclusions-These results suggest that the prevention of diabetic cardiomyopathy by zinc supplementation is predominantly mediated by an increase in cardiac MT. (Circulation. 2006;113:544-554.)

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Section: Discussionmentioning

confidence: 99%

Section: Supplementation With Znmentioning

confidence: 99%

Section: Assessment Of Left Ventricular Performancementioning

confidence: 99%

Section: Histopathological Examination By Light and Electron Microscopymentioning

confidence: 99%

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Cardiac Metallothionein Induction Plays the Major Role in the Prevention of Diabetic Cardiomyopathy by Zinc Supplementation

et al. 2006

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“…The diabetes literature is not fully consistent with respect to the effect of type 1 diabetes on the echocardiogram. Most studies using echocardiography in type 1 streptozotocin (STZ)-diabetic mouse models have shown significant left ventricular cardiac contractile dysfunction [29,30], while other studies did not find impaired contractility [31,32]. It is unclear why OVE26 hearts did not show basal cardiac dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Diabetic Cardiomyopathy in OVE26 Mice Shows Mitochondrial ROS Production and Divergence Between In Vivo and In Vitro Contractility

Song

Du²,

Prabhu³

et al. 2007

Rev Diabet Stud

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■ AbstractMany diabetic patients suffer from a cardiomyopathy that cannot be explained solely by poor coronary perfusion. This cardiomyopathy may be due to either organ-based damage like fibrosis, or to direct damage to cardiomyocytes. Mitochondrial-derived reactive oxygen species (ROS) have been proposed to contribute to this cardiomyopathy. To address these questions, we used the OVE26 mouse model of severe type 1 diabetes to measure contractility in isolated cardiomyocytes by edge detection and in vivo with echocardiography. We also assessed the source of ROS generation using both a general and a mitochondrial specific indicator. When contractility was assayed in freshly isolated myocytes, contraction was much stronger in control myocytes. However, contractility of normal myocytes became weaker during 24 hours of in vitro culture. In contrast, contractility of diabetic OVE26 myocytes remains stable during culture. Echocardiography revealed normal or hyperdynamic function in OVE26 hearts under basal conditions but with a sharply reduced response to isoproterenol, a β-adrenergic agonist. For ROS generation, we found that ROS production in diabetic myocytes was elevated after exposure to either high glucose or angiotensin II (AngII). Superoxide detection with the mitochondrial sensor MitoSOX Red confirmed that mitochondria are a major source of ROS generation in diabetic myocytes. These results show that contractile deficits in OVE26 diabetic hearts are due primarily to cardiomyocyte impairment and that ROS from mitochondria are a cause of that impairment.

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Animal Models of Diabetic Cardiomyopathy

Badole¹,

Jangam²

2015

Glucose Intake and Utilization in Pre-Diabetes and Diabetes

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Cardiac Functional Analysis by Electrocardiography, Echocardiography and in situ Hemodynamics in Streptozotocin-Induced Diabetic Mice

Cited by 12 publications

References 38 publications

Cardiac Metallothionein Induction Plays the Major Role in the Prevention of Diabetic Cardiomyopathy by Zinc Supplementation

Cardiac Metallothionein Induction Plays the Major Role in the Prevention of Diabetic Cardiomyopathy by Zinc Supplementation

Diabetic Cardiomyopathy in OVE26 Mice Shows Mitochondrial ROS Production and Divergence Between In Vivo and In Vitro Contractility

Animal Models of Diabetic Cardiomyopathy

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