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脂肪因子瘦素和脂联素在癫痫中的调控基础:从信号通路到糖代谢。

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism.

机构信息

Department of Neurology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, 215600, China.

Translational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, 215600, China.

出版信息

Neurochem Res. 2023 Jul;48(7):2017-2028. doi: 10.1007/s11064-023-03891-2. Epub 2023 Feb 16.

DOI:10.1007/s11064-023-03891-2
PMID:36797447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10181973/
Abstract

Epilepsy is a common and severe neurological disorder in which impaired glucose metabolism leads to changes in neuronal excitability that slow or promote the development of epilepsy. Leptin and adiponectin are important mediators regulating glucose metabolism in the peripheral and central nervous systems. Many studies have reported a strong association between epilepsy and these two adipokines involved in multiple signaling cascades and glucose metabolism. Due to the complex regulatory mechanisms between them and various signal activation networks, their role in epilepsy involves many aspects, including the release of inflammatory mediators, oxidative damage, and neuronal apoptosis. This paper aims to summarize the signaling pathways involved in leptin and adiponectin and the regulation of glucose metabolism from the perspective of the pathogenesis of epilepsy. In particular, we discuss the dual effects of leptin in epilepsy and the relationship between antiepileptic drugs and changes in the levels of these two adipokines. Clinical practitioners may need to consider these factors in evaluating clinical drugs. Through this review, we can better understand the specific involvement of leptin and adiponectin in the pathogenesis of epilepsy, provide ideas for further exploration, and bring about practical significance for the treatment of epilepsy, especially for the development of personalized treatment according to individual metabolic characteristics.

摘要

癫痫是一种常见且严重的神经系统疾病,其葡萄糖代谢受损导致神经元兴奋性改变,从而减缓或促进癫痫的发展。瘦素和脂联素是调节外周和中枢神经系统葡萄糖代谢的重要介质。许多研究报告称,癫痫与这两种参与多种信号级联和葡萄糖代谢的脂肪因子密切相关。由于它们之间存在复杂的调节机制和各种信号激活网络,它们在癫痫中的作用涉及多个方面,包括炎症介质的释放、氧化损伤和神经元凋亡。本文旨在从癫痫发病机制的角度,总结瘦素和脂联素涉及的信号通路及其对葡萄糖代谢的调节。特别是,我们讨论了瘦素在癫痫中的双重作用以及抗癫痫药物与这两种脂肪因子水平变化之间的关系。临床医生在评估临床药物时可能需要考虑这些因素。通过本次综述,我们可以更好地了解瘦素和脂联素在癫痫发病机制中的具体参与,为进一步探索提供思路,并为癫痫的治疗带来实际意义,特别是为根据个体代谢特征制定个性化治疗方案提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/10181973/dcf538881a7f/11064_2023_3891_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/10181973/45aa1ba937ed/11064_2023_3891_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/10181973/dcf538881a7f/11064_2023_3891_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/10181973/45aa1ba937ed/11064_2023_3891_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/10181973/dcf538881a7f/11064_2023_3891_Fig2_HTML.jpg

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