Article(id=1208795425784591046, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208795418612339683, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.10.16, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1614528000000, receivedDateStr=2021-03-01, revisedDate=1625846400000, revisedDateStr=2021-07-10, acceptedDate=null, acceptedDateStr=null, onlineDate=1766128887839, onlineDateStr=2025-12-19, pubDate=1635350400000, pubDateStr=2021-10-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766128887839, onlineIssueDateStr=2025-12-19, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766128887839, creator=13701087609, updateTime=1766128887839, updator=13701087609, issue=Issue{id=1208795418612339683, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='10', pageStart='955', pageEnd='1060', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766128886129, creator=13701087609, updateTime=1766128956061, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208795711982924071, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208795418612339683, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208795711982924072, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208795418612339683, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1051, endPage=1055, ext={EN=ArticleExt(id=1208795426883498704, articleId=1208795425784591046, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress in mechanism of IKKε and TBK1 in obesity, diabetes and NAFLD, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

TANK binding kinase 1 (TBK1) and IKKε, are new members of the IKK family. They are important regulators of nuclear factor κB (NF-κB) signaling pathway and play an important role in metabolic disease. IKKε and TBK1 not only reduce the sensitivity of β adrenergic receptors to catecholamines in adipocytes of obese mice, reduce the level of second messenger cAMP,but also regulate the regeneration of pancreatic β cells. Blocking the IKKε and TBK1 signaling pathways can promote adipose tissue energy consumption, reduce the expression of chronic inflammatory factors in adipocytes, enhance insulin sensitivity, reduce insulin resistance, reduce body weight, and prevent obesity caused by high fat diet. In this review, we reviewed the structure and function of TBK1 and IKKε, as well as the molecular mechanisms of TBK1 and IKKε in the regulation of metabolism in obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD). Finally, we discussed the potential of TBK1and IKKε in the treatment of metabolic diseases.

, correspAuthors=Xiu-Lan Zou, authorNote=null, correspAuthorsNote=, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, authorCompany=null, fund=null, authors=null, authorsList=Xiang-Hong Wang, Xiu-Lan Zou, Qian He), CN=ArticleExt(id=1208795427244208868, articleId=1208795425784591046, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=IKKε及TBK1在肥胖、糖尿病及NAFLD中的作用机制研究进展, columnId=1190243276029530637, journalTitle=解放军医学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

核因子κB激酶抑制剂ε(IKKε)及TANK结合激酶1(TBK1)是IKK家族中的新成员，是核因子κB(NF-κB)信号转导通路中的重要调节因子，在代谢性疾病中具有重要作用，不仅可降低肥胖小鼠脂肪细胞中的β肾上腺素受体对儿茶酚胺的敏感性及细胞内第二信使cAMP的水平，而且可调节胰腺β细胞的再生。阻断IKKε及TBK1信号通路可促进脂肪组织的能量消耗，减少脂肪细胞中慢性炎性因子的表达，增强胰岛素敏感性，减少胰岛素抵抗，减轻体重，防止高脂饮食引起的肥胖。该文综述了IKKε及TBK1的结构和功能，以及IKKε和TBK1在肥胖、2型糖尿病(T2DM)、非酒精性脂肪性肝病(NAFLD)中调节代谢的分子机制，并讨论了氨来占诺作为TBK1及IKKε抑制剂治疗代谢性疾病的潜力。

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王向红，硕士研究生。主要从事内分泌及代谢性疾病方面的研究

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王向红，硕士研究生。主要从事内分泌及代谢性疾病方面的研究

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