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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Dec 15, 2025; 16(12): 108609
Published online Dec 15, 2025. doi: 10.4239/wjd.v16.i12.108609
Published online Dec 15, 2025. doi: 10.4239/wjd.v16.i12.108609
Rheb1 signaling and the fate of pancreatic β cells: Toward a new frontier in diabetes therapy
Hadi Karimkhani, Medical Biochemistry, İstanbul Okan University, İstanbul 34959, Tuzla, Türkiye
Author contributions: Karimkhani H is the sole author and contributed to all aspects of the work, including conceptualization, literature review (investigation), methodology, visualization, writing the original draft, reviewing, and editing; Karimkhani H approved the final version and serves as the guarantor of the work.
Conflict-of-interest statement: The author declares that there is no conflict of interest regarding the publication of this article.
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: Hadi Karimkhani, PhD, Assistant Professor, Medical Biochemistry, İstanbul Okan University, Tepeören Mahallesi Tuzla Kampüsü, İstanbul 34959, Tuzla, Türkiye. drhadi.h@gmail.com
Received: April 18, 2025
Revised: August 13, 2025
Accepted: October 23, 2025
Published online: December 15, 2025
Processing time: 241 Days and 4.7 Hours
Revised: August 13, 2025
Accepted: October 23, 2025
Published online: December 15, 2025
Processing time: 241 Days and 4.7 Hours
Core Tip
Core Tip: Rheb1 is a critical regulator of pancreatic β cell survival and insulin secretion, acting through the mechanistic target of rapamycin complex 1 pathway to support β cell mass and function. This invited commentary evaluated how Rheb1-driven signaling modulates β cell fate and assesses its promise as a therapeutic target in diabetes. While enhancing Rheb1 activity could preserve or expand functional β cell mass, careful modulation is required to avoid unintended effects such as α cell overactivity. Understanding the dualistic nature of Rheb1 signaling in islet cell populations will be key to harnessing this pathway for future diabetes treatments.