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

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NEUROCHEMICAL RESEARCH
卷 -, 期 -, 页码 -

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SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-023-03891-2

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Adipokines; Leptin; Adiponectin; Epilepsy; Signaling pathways

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Epilepsy is a neurological disorder characterized by impaired glucose metabolism and changes in neuronal excitability. Leptin and adiponectin, as important regulators of glucose metabolism, have been found to be strongly associated with epilepsy. Their role in epilepsy involves various aspects such as inflammation, oxidative damage, and neuronal apoptosis. This paper aims to summarize the signaling pathways and regulation of glucose metabolism related to leptin and adiponectin in epilepsy. It also discusses the dual effects of leptin and the relationship between antiepileptic drugs and the levels of these two adipokines. Understanding their specific involvement in the pathogenesis of epilepsy has practical significance for the personalized treatment of epilepsy according to individual metabolic characteristics.
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.

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