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糖尿病小鼠脂肪组织中氧化应激增强,糖化白蛋白可能起作用。

Enhanced oxidative stress in adipose tissue from diabetic mice, possible contribution of glycated albumin.

作者信息

Boyer Florence, Diotel Nicolas, Girard Dorothée, Rondeau Philippe, Essop M Faadiel, Bourdon Emmanuel

机构信息

Inserm, UMR 1188 Diabète athérothrombose Thérapies Réunion Océan Indien (DéTROI), plateforme CYROI, Sainte-Clotilde F-97490, France; Université de La Réunion, UMR 1188, Sainte-Clotilde F-97490, France.

Cardio-Metabolic Research Group (CMRG), Department of Physiological Sciences, Stellenbosch University, Merriman Avenue, Stellenbosch 7600, South Africa.

出版信息

Biochem Biophys Res Commun. 2016 Apr 22;473(1):154-160. doi: 10.1016/j.bbrc.2016.03.068. Epub 2016 Mar 22.

DOI:10.1016/j.bbrc.2016.03.068
PMID:27012202
Abstract

Although enhanced oxidative stress and proteotoxicity constitute major contributors to the pathogenesis of multiple diseases, there is limited understanding of its role in adipose tissue. Here, we aimed at evaluating oxidative stress biomarkers in adipocytes from diabetic/obese db/db mice. The current study revealed that reactive oxygen species production was upregulated in adipocytes, together with lipid peroxidation 4-hydroxynonenal accumulation, and altered proteolytic and antioxidant activities. In parallel, acute exposure of 3T3L1 adipocyte cell lines to glycated albumin (known to be enhanced with diabetes) also elicited intracellular free radical formation. Our data provide novel insights into redox and proteolytic homeostasis in adipocytes.

摘要

尽管增强的氧化应激和蛋白毒性是多种疾病发病机制的主要促成因素,但人们对其在脂肪组织中的作用了解有限。在此,我们旨在评估糖尿病/肥胖db/db小鼠脂肪细胞中的氧化应激生物标志物。当前研究表明,脂肪细胞中的活性氧生成上调,同时脂质过氧化产物4-羟基壬烯醛积累,并且蛋白水解和抗氧化活性发生改变。同时,3T3L1脂肪细胞系急性暴露于糖化白蛋白(已知在糖尿病中会增加)也会引发细胞内自由基形成。我们的数据为脂肪细胞中的氧化还原和蛋白水解稳态提供了新的见解。

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