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Graf Isolan
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Untersuchte Arbeit:
Seite: 2, Zeilen: 6-20
Quelle: Poornima et al 2006
Seite(n): 597; 599, Zeilen: 597:left col. 4-13; 599:left col. 32ff
1.1.1 Cellular Mechanisms Predisposing Towards Diabetic Cardiomyopathy

There are 3 characteristic metabolic disturbances in diabetic states: hyperlipidaemia, early hyperinsulinaemia, followed by pancreatic β-cell failure and leading to hyperglycaemia. In this study, the animal model of diabetes refers to type 1 diabetes, which differs principally from type 2 diabetes in that it is unaccompanied by a period of hyperinsulinemia and is characterized by early-onset hyperglycaemia. Hyperglycaemia leads to increased glucose oxidation and mitochondrial generation of superoxide. In turn, excess superoxide leads to DNA damage and activation of poly (ADP ribose) polymerase (PARP) as a reparative enzyme [17]. PARP mediates the ribosylation and inhibition of glyceraldehydes phosphate dehydrogenase (GAPDH), which diverts glucose from its glycolytic pathway and into alternative biochemical pathways that are considered the mediators of hyperglycaemia-induced cellular injury. These consist of increases in advanced glycation end-products (AGEs), increased hexosamine and polyol flux and activation of classical isoforms of protein kinase C.


[17] Du, X.; Matsumura, T.; Edelstein, D.; Rossetti, L.; Zsenqeller, Z.; Szabo, C.; Brownlee, M. (2003): Inhibition of GAPDH activity by poly(ADB-ribose) polymerase, activates tree [sic] major pathways of hyperglycemic damage in endothelial cells, J.Clin.Invest. (volume 112), issue 7, pp. 1049-57. URL: PM:14523042

[Page 597]

Cellular Mechanisms Predisposing to Diabetic Cardiomyopathy

The 3 characteristic metabolic disturbances evident in diabetic states are hyperlipidemia (usually in the form of increased triglycerides and nonesterified fatty acids [NEFAs]) and early hyperinsulinemia followed by pancreatic β-cell failure, leading eventually to hyperglycemia. Type 1 diabetes differs principally from type 2 diabetes in that it is unaccompanied by a period of hyperinsulinemia and is characterized by early- as opposed to late-onset hyperglycemia.

[Page 599]

Hyperglycemia leads to increased glucose oxidation and mitochondrial generation of superoxide.37,39,40 In turn, excess superoxide leads to DNA damage and activation of poly (ADP ribose) polymerase (PARP) as a reparative enzyme.36 However, PARP also mediates the ribosylation and inhibition of glyceraldehyde phosphate dehydrogenase (GAPDH), diverting glucose from its glycolytic pathway and into alternative biochemical pathways that are considered the mediators of hyperglycemia induced cellular injury. These include increases in advanced glycation end products (AGEs), increased hexosamine and polyol flux, and activation of classical isoforms of protein kinase C.


36. Du X, Matsumura T, Edelstein D, Rossetti L, Zsengeller Z, Szabo C, Brownlee M. Inhibition of GAPDH activity by poly(ADB-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest.## 2003;112:1049–1057.

37. Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000;404:787–790.

39. Cai L, Kang YJ. Oxidative stress and diabetic cardiomyopathy: a brief review. Cardiovasc Toxicol. 2001;1:181–193.

40. Farhangkhoee H, Khan ZA, Mukherjee S, Cukiernik M, Barbin YP, Karmazyn M Chakrabarti S. Heme oxygenase in diabetes-induced oxidative stress in the heart. J Mol Cell Cardiol. 2003;35:1439–1448.

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