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神经病变与代谢综合征

Neuropathy and the metabolic syndrome.

作者信息

Piccolo Nicoló, Wiggers Astrid, Koubek Emily J, Feldman Eva L

机构信息

Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

eNeurologicalSci. 2024 Nov 28;38:100542. doi: 10.1016/j.ensci.2024.100542. eCollection 2025 Mar.

Abstract

Obesity and the metabolic syndrome (MetS) are major global health challenges that contribute significantly to the rising prevalence of type 2 diabetes (T2D) and neuropathy. Neuropathy, a common and disabling complication of T2D, is characterized by progressive distal-to-proximal axonal degeneration, driven in part by mitochondrial dysfunction in both neurons and axons. Recent evidence points to the toxic effects of saturated fatty acids on peripheral nerve health, with studies demonstrating that these fats impair mitochondrial function and bioenergetics, leading to distal axonal loss. Conversely, monounsaturated fatty acids are found to be neuroprotective, restoring mitochondrial function and preventing neuropathy. These findings suggest that dietary factors play a crucial role in the pathogenesis of neuropathy associated with metabolic dysregulation and emphasize the need for lifestyle interventions and therapies that target these newly identified mechanisms.

摘要

肥胖和代谢综合征是全球性的重大健康挑战,对2型糖尿病(T2D)和神经病变患病率的上升有显著影响。神经病变是T2D常见且致残的并发症,其特征是轴突从远端到近端进行性退化,部分原因是神经元和轴突中的线粒体功能障碍。最近的证据表明饱和脂肪酸对周围神经健康有毒性作用,研究表明这些脂肪会损害线粒体功能和生物能量学,导致远端轴突丧失。相反,发现单不饱和脂肪酸具有神经保护作用,可恢复线粒体功能并预防神经病变。这些发现表明饮食因素在与代谢失调相关的神经病变发病机制中起关键作用,并强调需要针对这些新发现机制的生活方式干预和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbc/11664003/6e40780112a8/gr1.jpg

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