cNPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes.

IF 4.2 3区医学 Q1 ENDOCRINOLOGY & METABOLISM

World Journal of Diabetes Pub Date : 2024-09-15 DOI:10.4239/wjd.v15.i9.1932

Yan-Bin Yin, Wei Ji, Ying-Lan Liu, Qian-Hao Gao, Dong-Dong He, Shi-Lin Xu, Jing-Xin Fan, Li-Hai Zhang

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引用次数: 0

Abstract

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.

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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。

背景：2型糖尿病（T2DM）是由胰岛素分泌缺陷和外周组织对胰岛素作用的抵抗所引起的。目的：探讨 T2DM 的发病机制，制定并实施新的 T2DM 预防和治疗策略：方法：采用接收者操作特征曲线（ROC）分析进行诊断标记。采用反转录-PCR 和 Western 印迹法测定基因的表达水平。通过细胞计数试剂盒-8（CCK-8）测试进行细胞增殖检测。最后，T2DM小鼠接受了Roux-en-Y胃旁路手术：结果：我们发现，NPAS2在T2DM小鼠胰岛β细胞凋亡中明显上调。ROC 曲线显示，NPAS2 能够准确诊断 T2DM。NPAS2 的过表达确实增加了 KANK1 的水平。此外，CCK-8试验显示，敲除NPAS2和KANK1会增加MIN6细胞的增殖。最后，我们发现胃旁路手术可通过下调 NPAS2 和 KANK1 治疗 2 型糖尿病：结论：本研究表明，NPAS2通过调控KANK1的表达诱导2型糖尿病患者β细胞功能障碍，它可能是T2DM的潜在治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

World Journal of Diabetes ENDOCRINOLOGY & METABOLISM-

自引率

2.40%

发文量

909

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.