{"title":"cNPAS2 通过调节 KANK1 的表达诱导 2 型糖尿病患者的 β 细胞功能障碍。","authors":"Yan-Bin Yin, Wei Ji, Ying-Lan Liu, Qian-Hao Gao, Dong-Dong He, Shi-Lin Xu, Jing-Xin Fan, Li-Hai Zhang","doi":"10.4239/wjd.v15.i9.1932","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus type 2 (T2DM) is formed by defective insulin secretion with the addition of peripheral tissue resistance of insulin action. It has been affecting over 400 million people all over the world.</p><p><strong>Aim: </strong>To explore the pathogenesis of T2DM and to develop and implement new prevention and treatment strategies for T2DM.</p><p><strong>Methods: </strong>Receiver operating characteristic (ROC) curve analysis was used to conduct diagnostic markers. The expression level of genes was determined by reverse transcription-PCR as well as Western blot. Cell proliferation assays were performed by cell counting kit-8 (CCK-8) tests. At last, T2DM mice underwent Roux-en-Y gastric bypass surgery.</p><p><strong>Results: </strong>We found that <i>NPAS2</i> was significantly up-regulated in islet β cell apoptosis of T2DM. The ROC curve revealed that <i>NPAS2</i> was capable of accurately diagnosing T2DM. <i>NPAS2</i> overexpression did increase the level of <i>KANK1</i>. In addition, the CCK-8 test revealed knocking down NPAS2 and KANK1 increased the proliferation of MIN6 cells. At last, we found that gastric bypass may treat type 2 diabetes by down-regulating <i>NPAS2</i> and <i>KANK1</i>.</p><p><strong>Conclusion: </strong>This study demonstrated that <i>NPAS2</i> induced β cell dysfunction by regulating <i>KANK1</i> expression in type 2 diabetes, and it may be an underlying therapy target of T2DM.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 9","pages":"1932-1941"},"PeriodicalIF":4.2000,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372636/pdf/","citationCount":"0","resultStr":"{\"title\":\"cNPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes.\",\"authors\":\"Yan-Bin Yin, Wei Ji, Ying-Lan Liu, Qian-Hao Gao, Dong-Dong He, Shi-Lin Xu, Jing-Xin Fan, Li-Hai Zhang\",\"doi\":\"10.4239/wjd.v15.i9.1932\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Diabetes mellitus type 2 (T2DM) is formed by defective insulin secretion with the addition of peripheral tissue resistance of insulin action. It has been affecting over 400 million people all over the world.</p><p><strong>Aim: </strong>To explore the pathogenesis of T2DM and to develop and implement new prevention and treatment strategies for T2DM.</p><p><strong>Methods: </strong>Receiver operating characteristic (ROC) curve analysis was used to conduct diagnostic markers. The expression level of genes was determined by reverse transcription-PCR as well as Western blot. Cell proliferation assays were performed by cell counting kit-8 (CCK-8) tests. At last, T2DM mice underwent Roux-en-Y gastric bypass surgery.</p><p><strong>Results: </strong>We found that <i>NPAS2</i> was significantly up-regulated in islet β cell apoptosis of T2DM. The ROC curve revealed that <i>NPAS2</i> was capable of accurately diagnosing T2DM. <i>NPAS2</i> overexpression did increase the level of <i>KANK1</i>. In addition, the CCK-8 test revealed knocking down NPAS2 and KANK1 increased the proliferation of MIN6 cells. At last, we found that gastric bypass may treat type 2 diabetes by down-regulating <i>NPAS2</i> and <i>KANK1</i>.</p><p><strong>Conclusion: </strong>This study demonstrated that <i>NPAS2</i> induced β cell dysfunction by regulating <i>KANK1</i> expression in type 2 diabetes, and it may be an underlying therapy target of T2DM.</p>\",\"PeriodicalId\":48607,\"journal\":{\"name\":\"World Journal of Diabetes\",\"volume\":\"15 9\",\"pages\":\"1932-1941\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2024-09-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11372636/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"World Journal of Diabetes\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.4239/wjd.v15.i9.1932\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"World Journal of Diabetes","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4239/wjd.v15.i9.1932","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
cNPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes.
Background: Diabetes mellitus type 2 (T2DM) is formed by defective insulin secretion with the addition of peripheral tissue resistance of insulin action. It has been affecting over 400 million people all over the world.
Aim: To explore the pathogenesis of T2DM and to develop and implement new prevention and treatment strategies for T2DM.
Methods: Receiver operating characteristic (ROC) curve analysis was used to conduct diagnostic markers. The expression level of genes was determined by reverse transcription-PCR as well as Western blot. Cell proliferation assays were performed by cell counting kit-8 (CCK-8) tests. At last, T2DM mice underwent Roux-en-Y gastric bypass surgery.
Results: We found that NPAS2 was significantly up-regulated in islet β cell apoptosis of T2DM. The ROC curve revealed that NPAS2 was capable of accurately diagnosing T2DM. NPAS2 overexpression did increase the level of KANK1. In addition, the CCK-8 test revealed knocking down NPAS2 and KANK1 increased the proliferation of MIN6 cells. At last, we found that gastric bypass may treat type 2 diabetes by down-regulating NPAS2 and KANK1.
Conclusion: This study demonstrated that NPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes, and it may be an underlying therapy target of T2DM.
期刊介绍：
The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.
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