Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Sep 15, 2024; 15(9): 1932-1941
Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1932
cNPAS2 induced β cell dysfunction by regulating KANK1 expression in type 2 diabetes
Yan-Bin Yin, Wei Ji, Ying-Lan Liu, Qian-Hao Gao, Dong-Dong He, Shi-Lin Xu, Jing-Xin Fan, Li-Hai Zhang
Yan-Bin Yin, Shi-Lin Xu, Li-Hai Zhang, Department of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, Heilongjiang Province, China
Wei Ji, Department of Anesthesiology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264199, Shandong Province, China
Ying-Lan Liu, Operating Room, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, Heilongjiang Province, China
Qian-Hao Gao, Department of Anesthesiology, Huazhong University of Science and Technology Union Jiangbei Hospital, Wuhan 430100, Hubei Province, China
Dong-Dong He, Jing-Xin Fan, Department of Endocrinology, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, Heilongjiang Province, China
Co-first authors: Yan-Bin Yin and Wei Ji.
Author contributions: Yin YB, Zhang LH and Ji W were responsible for conception and design; He DD, Fan JX were responsible for administrative support; Xu SL, Gao QH, He DD and Fan JX were responsible for provision of study materials or patients; Zhang LH and Gao QH were responsible for collection and assembly of data; Zhang LH and Yin YB were responsible for data analysis and interpretation; all authors were responsible for manuscript writing; all authors were responsible for final approval of manuscript.
Supported by Natural Science Foundation of Heilongjiang Province, No. LH2021H105.
Institutional animal care and use committee statement: The animal investigation described in this report was approved by the Biological and Medical Research Ethics Committee of Jiamusi University (No. 2021-0330).
Conflict-of-interest statement: The authors have no relevant financial or non-financial interests to disclose.
Data sharing statement: The datasets generated and/or analysed during the current study are available in the manuscript and supp lementary materials.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Li-Hai Zhang, MSc, Associate Chief Physician, Department of General Surgery, The First Affiliated Hospital of Jiamusi University, No. 348 Dexiang Street, Xiangyang District, Jiamusi 154000, Heilongjiang Province, China. zhanglihai@jmsu.edu.cn
Received: April 10, 2024
Revised: June 17, 2024
Accepted: July 18, 2024
Published online: September 15, 2024
Processing time: 139 Days and 6.6 Hours
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.

Keywords: Diabetes mellitus type 2; KANK1; NPAS2; Gastric bypass

Core Tip: Diabetes mellitus type 2 (T2DM) is formed by defective insulin secretion with the addition of peripheral tissue resistance of insulin action. 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.