Suppr超能文献

酮体在糖尿病性痴呆中的作用:沉默调节蛋白、胰岛素抵抗、突触可塑性、线粒体功能障碍和神经递质。

Role of ketone bodies in diabetes-induced dementia: sirtuins, insulin resistance, synaptic plasticity, mitochondrial dysfunction, and neurotransmitter.

机构信息

Department of Neurology, Chosun University Medical School, Gwangju, Republic of Korea.

Department of Food Science and Nutrition and the Department of Health Sciences, Dong-A University, Busan, Republic of Korea.

出版信息

Nutr Rev. 2022 Mar 10;80(4):774-785. doi: 10.1093/nutrit/nuab118.

Abstract

Patients with type 2 diabetes can have several neuropathologies, such as memory deficits. Recent studies have focused on the association between metabolic imbalance and neuropathological problems, and the associated molecular pathology. Diabetes triggers neuroinflammation, impaired synaptic plasticity, mitochondrial dysfunction, and insulin resistance in the brain. Glucose is a main energy substrate for neurons, but under certain conditions, such as fasting and starvation, ketone bodies can be used as an energy fuel for these cells. Recent evidence has shed new light on the role of ketone bodies in regulating several anti-inflammation cellular pathways and improving glucose metabolism, insulin action, and synaptic plasticity, thereby being neuroprotective. However, very high amount of ketone bodies can be toxic for the brain, such as in ketoacidosis, a dangerous complication that may occur in type 1 diabetes mellitus or alcoholism. Recent findings regarding the relationship between ketone bodies and neuropathogenesis in dementia are reviewed in this article. They suggest that the adequately low amount of ketone bodies can be a potential energy source for the treatment of diabetes-induced dementia neuropathology, considering the multifaceted effects of the ketone bodies in the central nervous system. This review can provide useful information for establishing the therapeutic guidelines of a ketogenic diet for diabetes-induced dementia.

摘要

2 型糖尿病患者可能存在多种神经病理学问题,如记忆缺陷。最近的研究集中在代谢失衡与神经病理学问题以及相关的分子病理学之间的关联上。糖尿病会在大脑中引发神经炎症、突触可塑性受损、线粒体功能障碍和胰岛素抵抗。葡萄糖是神经元的主要能量底物,但在某些情况下,如禁食和饥饿时,酮体可以作为这些细胞的能量燃料。最近的证据揭示了酮体在调节几种抗炎细胞途径以及改善葡萄糖代谢、胰岛素作用和突触可塑性方面的作用,从而具有神经保护作用。然而,非常高的酮体含量可能对大脑有毒,例如在酮症酸中毒中,这是一种可能发生在 1 型糖尿病或酒精中毒中的危险并发症。本文综述了最近关于酮体与痴呆症神经发病机制之间关系的研究结果。它们表明,适量的酮体可以成为治疗糖尿病引起的痴呆症神经病理学的潜在能量来源,考虑到酮体在中枢神经系统中的多方面作用。这篇综述可以为制定治疗糖尿病引起的痴呆症的生酮饮食治疗指南提供有用信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77cb/8907488/2f13df90439e/nuab118f1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验