脂肪因子与神经性厌食症作用机制的研究进展

Research progress on the mechanism of Adipokines and Anorexia Nervosa

ES评分 0

DOI
刊名
Journal of International Psychiatry
年,卷(期) 2023, 50(6)
作者
作者单位

滨州医学院附属医院 ;

摘要
神经性厌食症(Anorexia nervosa,AN)是一种由各种病理和生理因素引起的对食物失去欲望的一种疾病。脂联素和瘦素是脂肪细胞分泌的蛋白质,脂联素可以通过腺苷单磷酸蛋白激酶(AMPK)和磷酸肌醇3-激酶(PI3K)通路调节下丘脑弓状核的神经肽Y(NPY)、刺鼠相关肽(AgRP)和阿片黑皮质素原(POMC)神经元活性调控食物摄入;瘦素可以通过调控JAK2(Janus激酶2)-STAT3(信号转导和转录激活子3)、PI3K和AMPK通路调节下丘脑摄食相关神经元活性调控食物摄入。目前研究发现脂联素和瘦素与AN发病有一定关系。与健康人相比,AN患者脑脊液中的脂联素和瘦素水平发生了变化。脂联素和瘦素可能为治疗厌食症提供一个新的思路,这篇文章对脂联素与神经性厌食症作用机制做一综述。
Abstract
Anorexia nervosa is a disease of loss of desire for food caused by various pathological and physiological factors. Adiponectin and leptin are proteins secreted by adipocytes, and adiponectin can regulate the neuropeptide Y (NPY) of the arcuate nucleus of the hypothalamus through the adenosine monophosphate protein kinase (AMPK) and phosphoinositide 3-kinase (PI3K) pathways. ), agouti-related peptide (AgRP), and pro-opioid melanocortin (POMC) neuronal activity regulate food intake; leptin can regulate food intake by regulating JAK2 (Janus kinase 2)-STAT3 (signal transducer and activator of transcription 3), PI3K and AMPK pathways regulate food intake by regulating the activity of hypothalamic feeding-related neurons. Current studies have found that adiponectin and leptin have a certain relationship with the pathogenesis of AN. The levels of adiponectin and leptin in the cerebrospinal fluid of patients with AN were altered compared with healthy individuals. Adiponectin and leptin may provide a new idea for the treatment of anorexia. This article reviews the mechanism of adiponectin and anorexia nervosa.
关键词
神经性厌食症;脂联素;瘦素;饮食
KeyWord
Anorexia nervosa;Adiponectin;leptin;diet
基金项目
页码 1267-1271
  • 参考文献
  • 相关文献
  • 引用本文

杨梦雨,张浩,傅晓凤,王雪贞*,韩笑峰,陈超. 脂肪因子与神经性厌食症作用机制的研究进展 [J]. 国际精神病学杂志. 2023; 50; (6). 1267 - 1271.

  • 文献评论

相关学者

相关机构