Inflammatory cause of metabolic syndrome via brain stress and NF-κB.
Inflammatory cause of metabolic syndrome via brain stress and NF-κB.
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DOI：
10.18632/aging.100431
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发表时间：
2012-02
期刊：
影响因子：
--
通讯作者：
Liu T
中科院分区：
文献类型：
--
作者：
Cai D;Liu T
代谢综合征是一种医学疾病网络，大大增加了发展代谢和心血管疾病的风险，在当今世界的许多地区已经达到流行病的程度。尽管医疗状况令人担忧，但对代谢综合征的根本机制的科学认识仍然有限，这种知识不足导致相关疾病的有效治疗或预防相对缺乏。最近神经内分泌学和神经免疫学领域的跨学科研究表明，营养过剩可以触发细胞内应激，引起由控制先天免疫的分子介导的炎症变化。中枢神经系统（特别是下丘脑）中的这种类型的营养相关分子炎症可以形成诱导各种代谢综合征成分（例如肥胖、胰岛素抵抗和高血压）的共同致病基础。NF-κB通路是脑炎症病理诱导的关键分子系统，它将营养过剩和细胞内应激转化为中枢神经内分泌和神经系统能量、血糖和心血管稳态的失调，共同导致代谢综合征。本文从细胞内应激的致病诱导和脑内NF-κB通路的角度综述了代谢综合征及其相关疾病的神经机制的研究进展。
Metabolic syndrome, a network of medical disorders that greatly increase the risk for developing metabolic and cardiovascular diseases, has reached epidemic levels in many areas of today's world. Despite this alarming medicare situation, scientific understandings on the root mechanisms of metabolic syndrome are still limited, and such insufficient knowledge contributes to the relative lack of effective treatments or preventions for related diseases. Recent interdisciplinary studies from neuroendocrinology and neuroimmunology fields have revealed that overnutrition can trigger intracellular stresses to cause inflammatory changes mediated by molecules that control innate immunity. This type of nutrition-related molecular inflammation in the central nervous system, particularly in the hypothalamus, can form a common pathogenic basis for the induction of various metabolic syndrome components such as obesity, insulin resistance, and hypertension. Proinflammatory NF-κB pathway has been revealed as a key molecular system for pathologic induction of brain inflammation, which translates overnutrition and resulting intracellular stresses into central neuroendocrine and neural dysregulations of energy, glucose, and cardiovascular homeostasis, collectively leading to metabolic syndrome. This article reviews recent research advances in the neural mechanisms of metabolic syndrome and related diseases from the perspective of pathogenic induction by intracellular stresses and NF-κB pathway of the brain.
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