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炎症与氧化应激:胰岛素抵抗、肥胖症和阿尔茨海默病之间的分子联系

Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease.

作者信息

Verdile Giuseppe, Keane Kevin N, Cruzat Vinicius F, Medic Sandra, Sabale Miheer, Rowles Joanne, Wijesekara Nadeeja, Martins Ralph N, Fraser Paul E, Newsholme Philip

机构信息

School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia ; Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA 6027, Australia.

School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

出版信息

Mediators Inflamm. 2015;2015:105828. doi: 10.1155/2015/105828. Epub 2015 Nov 26.

Abstract

Type 2 diabetes (T2DM), Alzheimer's disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer's disease (AD) is the most common subtype of dementia. Reduced release (for T2DM) and decreased action of insulin are central to the development and progression of both T2DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T2DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic inflammatory response and oxidative stress associated with T2DM, amyloid-β (Aβ) protein accumulation, and mitochondrial dysfunction link T2DM and AD.

摘要

2型糖尿病(T2DM)、阿尔茨海默病(AD)和胰岛素抵抗都是与年龄相关的病症,其患病率上升受到公众关注。最近的研究表明,胰岛素抵抗和胰岛素信号传导受损可能是糖尿病、痴呆症和其他神经疾病进展的一个促成因素。阿尔茨海默病(AD)是痴呆症最常见的亚型。胰岛素释放减少(对于2型糖尿病而言)以及胰岛素作用减弱是2型糖尿病和AD发生及进展的核心。进行了文献检索以确定肥胖、糖尿病和AD之间的分子共性。胰岛素抵抗通过胰岛素信号传导受损或通过血液中葡萄糖和脂质(胆固醇和三酰甘油)代谢及浓度的异常变化影响许多组织和器官。尽管流行病学和生物学证据突出了2型糖尿病患者认知功能下降和AD发病率增加的情况,但细胞和组织功能障碍的共同分子基础正迅速得到认可。作为原因或结果,与2型糖尿病相关的慢性炎症反应和氧化应激、淀粉样β(Aβ)蛋白积累以及线粒体功能障碍将2型糖尿病和AD联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9a7/4674598/18767b8c9aa6/MI2015-105828.001.jpg

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