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C 反应蛋白在糖尿病炎症中的作用。

Role of C-Reactive Protein in Diabetic Inflammation.

机构信息

Department of Radiobiology and Molecular Genetics, VINČA Institute of Nuclear Sciences-National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.

King Abdullah University of Science and Technology (KAUST), Computer, Electrical, and Mathematical Sciences and Engineering (CEMSE) Division, Computational Bioscience Research Center (CBRC), Thuwal, Saudi Arabia.

出版信息

Mediators Inflamm. 2022 May 17;2022:3706508. doi: 10.1155/2022/3706508. eCollection 2022.

DOI:10.1155/2022/3706508
PMID:35620114
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9129992/
Abstract

Even though type 2 diabetes mellitus (T2DM) represents a worldwide chronic health issue that affects about 462 million people, specific underlying determinants of insulin resistance (IR) and impaired insulin secretion are still unknown. There is growing evidence that chronic subclinical inflammation is a triggering factor in the origin of T2DM. Increased C-reactive protein (CRP) levels have been linked to excess body weight since adipocytes produce tumor necrosis factor (TNF-) and interleukin 6 (IL-6), which are pivotal factors for CRP stimulation. Furthermore, it is known that hepatocytes produce relatively low rates of CRP in physiological conditions compared to T2DM patients, in which elevated levels of inflammatory markers are reported, including CRP. CRP also participates in endothelial dysfunction, the production of vasodilators, and vascular remodeling, and increased CRP level is closely associated with vascular system pathology and metabolic syndrome. In addition, insulin-based therapies may alter CRP levels in T2DM. Therefore, determining and clarifying the underlying CRP mechanism of T2DM is imperative for novel preventive and diagnostic procedures. Overall, CRP is one of the possible targets for T2DM progression and understanding the connection between insulin and inflammation may be helpful in clinical treatment and prevention approaches.

摘要

尽管 2 型糖尿病(T2DM)是一种影响全球约 4.62 亿人的慢性健康问题,但胰岛素抵抗(IR)和胰岛素分泌受损的确切潜在决定因素仍不清楚。越来越多的证据表明,慢性亚临床炎症是 T2DM 发病的一个触发因素。由于脂肪细胞产生肿瘤坏死因子(TNF-)和白细胞介素 6(IL-6),导致 C 反应蛋白(CRP)水平升高与超重有关,而 TNF- 和 IL-6 是 CRP 刺激的关键因素。此外,已知与生理条件相比,肝细胞在 T2DM 患者中产生相对较低水平的 CRP,在 T2DM 患者中报告了炎症标志物水平升高,包括 CRP。CRP 还参与内皮功能障碍、血管舒张剂的产生和血管重塑,并且 CRP 水平升高与血管系统病理学和代谢综合征密切相关。此外,基于胰岛素的治疗方法可能会改变 T2DM 患者的 CRP 水平。因此,确定和阐明 T2DM 中 CRP 的潜在机制对于新的预防和诊断程序至关重要。总的来说,CRP 是 T2DM 进展的可能靶点之一,了解胰岛素和炎症之间的联系可能有助于临床治疗和预防方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701b/9129992/574d49629ed4/MI2022-3706508.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701b/9129992/072ab350d3bf/MI2022-3706508.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701b/9129992/574d49629ed4/MI2022-3706508.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701b/9129992/072ab350d3bf/MI2022-3706508.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701b/9129992/574d49629ed4/MI2022-3706508.002.jpg

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