JAK-STAT and feeding.

JAK-STAT Pub Date : 2013-04-01 DOI:10.4161/jkst.23675
Sharon R Ladyman, David R Grattan
{"title":"JAK-STAT and feeding.","authors":"Sharon R Ladyman,&nbsp;David R Grattan","doi":"10.4161/jkst.23675","DOIUrl":null,"url":null,"abstract":"<p><p>The regulation of energy balance requires a complex system to homeostatically maintain the adult body at a precise set point. The central nervous system, particularly the hypothalamus, plays a key role in integrating a variety of signals that can relay information about the body's energy stores. As part of this system, numerous cytokines and hormones contribute to the regulation of food intake and energy homeostasis. Cytokines, and some hormones, are known to act through JAK-STAT intracellular signaling pathways. The hormone leptin, which plays a vital role in appetite regulation, signals through the JAK-STAT pathway, and it is through this involvement that the JAK-STAT pathway has become an established component in the mechanisms regulating food intake within the body. Emerging research, however, is now showing that this involvement of JAK-STAT is not limited to its activation by leptin. Furthermore, while the JAK-STAT pathway may simply act to transmit the anorectic signal of circulating factors, this intracellular signaling pathway may also become impaired when normal regulation of energy balance is disrupted. Thus, altered JAK-STAT signaling may contribute to the breakdown of the normal homeostatic mechanisms maintaining body weight in obesity. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23675"},"PeriodicalIF":0.0000,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23675","citationCount":"35","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JAK-STAT","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4161/jkst.23675","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 35

Abstract

The regulation of energy balance requires a complex system to homeostatically maintain the adult body at a precise set point. The central nervous system, particularly the hypothalamus, plays a key role in integrating a variety of signals that can relay information about the body's energy stores. As part of this system, numerous cytokines and hormones contribute to the regulation of food intake and energy homeostasis. Cytokines, and some hormones, are known to act through JAK-STAT intracellular signaling pathways. The hormone leptin, which plays a vital role in appetite regulation, signals through the JAK-STAT pathway, and it is through this involvement that the JAK-STAT pathway has become an established component in the mechanisms regulating food intake within the body. Emerging research, however, is now showing that this involvement of JAK-STAT is not limited to its activation by leptin. Furthermore, while the JAK-STAT pathway may simply act to transmit the anorectic signal of circulating factors, this intracellular signaling pathway may also become impaired when normal regulation of energy balance is disrupted. Thus, altered JAK-STAT signaling may contribute to the breakdown of the normal homeostatic mechanisms maintaining body weight in obesity.

Abstract Image

JAK-STAT和喂食。
能量平衡的调节需要一个复杂的系统来维持成人身体在一个精确的设定点。中枢神经系统,特别是下丘脑,在整合各种信号方面起着关键作用,这些信号可以传递有关身体能量储存的信息。作为这个系统的一部分,许多细胞因子和激素有助于调节食物摄入和能量稳态。已知细胞因子和一些激素通过JAK-STAT细胞内信号通路起作用。瘦素激素在食欲调节中起着至关重要的作用,它通过JAK-STAT通路发出信号,正是通过这种参与,JAK-STAT通路已经成为调节体内食物摄入机制的一个既定组成部分。然而,新兴的研究表明,JAK-STAT的参与并不局限于瘦素的激活。此外,虽然JAK-STAT通路可能只是传递循环因子的厌食信号,但当正常的能量平衡调节被破坏时,这种细胞内信号通路也可能受损。因此,改变的JAK-STAT信号可能导致正常的体内平衡机制的破坏,从而维持肥胖患者的体重。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书