Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. May 15, 2024; 15(5): 814-817
Published online May 15, 2024. doi: 10.4239/wjd.v15.i5.814
Glucokinase regulatory protein rs780094 polymorphism is associated with type 2 diabetes mellitus, dyslipidemia, non-alcoholic fatty liver disease, and nephropathy
Ashraf Al Madhoun
Ashraf Al Madhoun, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15400, Kuwait
Author contributions: Al Madhoun A designed the overall concept, review of literature, writing, and editing the manuscript.
Supported by the Kuwait Foundation for the Advancement of Sciences (KFAS) and Dasman Diabetes Institute, No. RACB-2021-007.
Conflict-of-interest statement: The authors declare that they have no conflict of interest to disclose.
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: Ashraf Al Madhoun, PhD, Academic Editor, Senior Scientist, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Jassim AlBahar Street, Dasman 15400, Kuwait. ashraf.madhoun@dasmaninstitute.org
Received: December 4, 2023
Peer-review started: December 4, 2023
First decision: January 23, 2024
Revised: January 31, 2024
Accepted: March 11, 2024
Article in press: March 11, 2024
Published online: May 15, 2024
Processing time: 157 Days and 21 Hours
Core Tip

Core Tip: Genome-wide association studies have identified the glucokinase regulatory protein rs780094 variant as a risk factor for type 2 diabetes mellitus and its associated dyslipidemia, non-alcoholic fatty liver disease, and nephropathy. The precise mechanism of action remains elusive. Clinical evidence suggests that the variant impairs pancreatic β-cell function and disrupts hepatic triglyceride and glucose metabolism across various ethnicities.