Experimental diabetes and left ventricular hypertrophy

Grimm, Daniela; Jabusch, Hans C.; Koßmehl, Peter; Huber, Michaela; Fredersdorf, Sabine; Griese, Daniel P.; Krämer, Bernhard K.; Kromer, Eckhard P.

doi:10.1016/s1054-8807(01)00116-8

Cited by 38 publications

(24 citation statements)

References 36 publications

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“…32,33) Our results are in accordance with the previous findings, 14,15,34) where the levels of TGFb1 and collagen III have been shown to be increased in diabetes-induced cardiac hypertrophy and fibrosis. In this study, the percentage of cardiac myocyte fibrosis as well as the expression of cytokine TGFb1 and extra cellular fiber collagen III were significantly elevated in the left ventricle of TG mice relative to NTG mice 28 and 56 d after STZ injection; which indicates that experimental diabetes-induced cardiac fibrosis is intensified in DN-14-3-3 mice.…”

Section: Discussionsupporting

confidence: 92%

Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C .BETA.2 in Experimental Diabetes

Narasimman

Watanabe

et al. 2005

Biological & Pharmaceutical Bulletin

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Section: Discussionsupporting

confidence: 92%

Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C .BETA.2 in Experimental Diabetes

Narasimman

Watanabe

et al. 2005

Biological & Pharmaceutical Bulletin

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“…One of the cardiac phenotypic manifestations of the streptozotocin rat model of diabetes is LV hypertrophy [41]. Diabetes leads to an increase in LV myocardial mass both in the presence [42] and absence of hypertension [43].…”

Section: Discussionmentioning

confidence: 99%

Characterization of Alterations in Diabetic Myocardial Tissue Using High Resolution MRI

Loganathan

Bilgen

Al-Hafez

et al. 2005

Int J Cardiovasc Imaging

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Cardiovascular complications, including diabetic cardiomyopathy, are the major cause of fatalities in diabetes. Diabetic cardiomyopathy is expressed in part through fibrosis and left ventricular hypertrophy, increasing myocardial stiffness leading to heart failure. In order to search for curative interventions, precise evaluation of the diabetic heart pathology is extremely important. Magnetic resonance imaging (MRI) is ideally suited for the assessment of heart disorders due to its high resolution, three-dimensional properties and dimensional accuracy. In this study streptozotocin injected Sprague-Dawley rats were used as a model of type 1 diabetes to characterize abnormalities in the diabetic left ventricle (LV). High resolution MRI using a 9.4 T horizontal bore scanner was performed on control and 7 weeks diabetic rats. In the diabetic rats as compared to controls, we found increased LV wall volume to body weight ratio, suggestive of LV hypertrophy; increased LV wall mean pixel intensity, and decreased T2 relaxation time, both suggestive of changes in the diabetic tissue properties, perhaps due to presence of fibrosis which was detected through increase in the collagen fractional area. In addition, changes in the LV cavity area were observed and quantified in post-mortem diabetic hearts indicative of stiffer and less resilient LV myocardial tissue with diabetes. Together the data suggest that LV hypertrophy and fibrosis may be a major factor underlying structural and functional abnormalities in the diabetic heart, and MRI is a valuable tool to non-invasively monitor the pathological changes in diabetic cardiomyopathy.

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“…Thus, trientine improved cellular histology in diabetes, consistent with the functional recovery. Untreated diabetes increased type I collagen (35,36), but trientine-treated diabetes did not differ from controls (Table 2). Untreated diabetes also increased type III collagen (37), which was normalized by trientine (Table 2).…”

Section: Figmentioning

confidence: 94%

Regeneration of the Heart in Diabetes by Selective Copper Chelation

et al. 2004

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Heart disease is the major cause of death in diabetes, a disorder characterized by chronic hyperglycemia and cardiovascular complications. Although altered systemic regulation of transition metals in diabetes has been the subject of previous investigation, it is not known whether changed transition metal metabolism results in heart disease in common forms of diabetes and whether metal chelation can reverse the condition. We found that administration of the Cu-selective transition metal chelator trientine to rats with streptozotocin-induced diabetes caused increased urinary Cu excretion compared with matched controls. A Cu II -trientine complex was demonstrated in the urine of treated rats. In diabetic animals with established heart failure, we show here for the first time that 7 weeks of oral trientine therapy significantly alleviated heart failure without lowering blood glucose, substantially improved cardiomyocyte structure, and reversed elevations in left ventricular collagen and ␤ 1 integrin. Oral trientine treatment also caused elevated Cu excretion in humans with type 2 diabetes, in whom 6 months of treatment caused elevated left ventricular mass to decline significantly toward normal. These data implicate accumulation of elevated loosely bound Cu in the mechanism of cardiac damage in diabetes and support the use of selective Cu chelation in the treatment of this condition.

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Experimental diabetes and left ventricular hypertrophy

Cited by 38 publications

References 36 publications

Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C .BETA.2 in Experimental Diabetes

Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C .BETA.2 in Experimental Diabetes

Characterization of Alterations in Diabetic Myocardial Tissue Using High Resolution MRI

Regeneration of the Heart in Diabetes by Selective Copper Chelation

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