Author: Brouwers Olaf de Vos-Houben Joyce M. J. Niessen Petra M. G. Miyata Toshio van Nieuwenhoven Frans Janssen Ben J. A. Hageman Geja Stehouwer Coen D. A. Schalkwijk Casper G.
Publisher: MDPI
E-ISSN: 1422-0067|14|8|15724-15739
ISSN: 1422-0067
Source: International Journal of Molecular Sciences, Vol.14, Iss.8, 2013-07, pp. : 15724-15739
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Abstract
Diabetes significantly increases the risk of heart failure. The increase in advanced glycation endproducts (AGEs) and oxidative stress have been associated with diabetic cardiomyopathy. We recently demonstrated that there is a direct link between AGEs and oxidative stress. Therefore, the aim of the current study was to investigate if a reduction of AGEs by overexpression of the glycation precursor detoxifying enzyme glyoxalase-I (GLO-I) can prevent diabetes-induced oxidative damage, inflammation and fibrosis in the heart. Diabetes was induced in wild-type and GLO-I transgenic rats by streptozotocin. After 24-weeks of diabetes, cardiac function was monitored with ultrasound under isoflurane anesthesia. Blood was drawn and heart tissue was collected for further analysis. Analysis with UPLC-MSMS showed that the AGE Nɛ-(1-carboxymethyl)lysine and its precursor 3-deoxyglucosone were significantly elevated in the diabetic hearts. Markers of oxidative damage, inflammation, and fibrosis were mildly up-regulated in the heart of the diabetic rats and were attenuated by GLO-I overexpression. In this model of diabetes, these processes were not accompanied by significant changes in systolic heart function,
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