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氧化应激与脂肪细胞生物学:聚焦晚期糖基化终末产物的作用

Oxidative stress and adipocyte biology: focus on the role of AGEs.

作者信息

Boyer Florence, Vidot Jennifer Baraka, Dubourg Alexis Guerin, Rondeau Philippe, Essop M Faadiel, Bourdon Emmanuel

机构信息

UMR DéTROI, Inserm U1188 Diabète Athérothrombose Thérapies Réunion Océan Indien, Université de La Réunion, Plateforme CYROI, Saint Denis de La Réunion, France.

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

出版信息

Oxid Med Cell Longev. 2015;2015:534873. doi: 10.1155/2015/534873. Epub 2015 Mar 23.

DOI:10.1155/2015/534873
PMID:25878764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4386674/
Abstract

Diabetes is a major health problem that is usually associated with obesity, together with hyperglycemia and increased advanced glycation endproducts (AGEs) formation. Elevated AGEs elicit severe downstream consequences via their binding to receptors of AGEs (RAGE). This includes oxidative stress and oxidative modifications of biological compounds together with heightened inflammation. For example, albumin (major circulating protein) undergoes increased glycoxidation with diabetes and may represent an important biomarker for monitoring diabetic pathophysiology. Despite the central role of adipose tissue in many physiologic/pathologic processes, recognition of the effects of greater AGEs formation in this tissue is quite recent within the obesity/diabetes context. This review provides a brief background of AGEs formation and adipose tissue biology and thereafter discusses the impact of AGEs-adipocyte interactions in pathology progression. Novel data are included showing how AGEs (especially glycated albumin) may be involved in hyperglycemia-induced oxidative damage in adipocytes and its potential links to diabetes progression.

摘要

糖尿病是一个主要的健康问题,通常与肥胖、高血糖以及晚期糖基化终产物(AGEs)生成增加有关。升高的AGEs通过与AGEs受体(RAGE)结合引发严重的下游后果。这包括氧化应激、生物化合物的氧化修饰以及炎症加剧。例如,白蛋白(主要的循环蛋白)在糖尿病患者中糖氧化增加,可能是监测糖尿病病理生理过程的重要生物标志物。尽管脂肪组织在许多生理/病理过程中起着核心作用,但在肥胖/糖尿病背景下,认识到该组织中AGEs生成增加所产生的影响却是最近才有的事。本综述提供了AGEs生成和脂肪组织生物学的简要背景,随后讨论了AGEs - 脂肪细胞相互作用在病理进展中的影响。还纳入了新数据,展示了AGEs(尤其是糖化白蛋白)如何参与高血糖诱导的脂肪细胞氧化损伤及其与糖尿病进展的潜在联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/052d4dda6b01/OMCL2015-534873.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/86e28c52b768/OMCL2015-534873.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/b87341b3ddfd/OMCL2015-534873.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/f8aa1755ee97/OMCL2015-534873.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/052d4dda6b01/OMCL2015-534873.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/86e28c52b768/OMCL2015-534873.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/b87341b3ddfd/OMCL2015-534873.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/f8aa1755ee97/OMCL2015-534873.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8829/4386674/052d4dda6b01/OMCL2015-534873.004.jpg

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