Gouda MM. Rheb1 as a novel β-cell regulator connecting mTORC1, AMPK, and NOTCH1 pathways for efficient diabetes therapy. World J Diabetes 2025; 16(8): 108310 [DOI: 10.4239/wjd.v16.i8.108310]
Corresponding Author of This Article
Mostafa M Gouda, PhD, Professor, College of Biosystems Engineering and Food Science, Zhejiang University, No. 866 Yuhangtang Road, Hangzhou 310058, Zhejiang Province, China. mostafa-gouda@zju.edu.cn
Research Domain of This Article
Chemistry, Medicinal
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Aug 15, 2025; 16(8): 108310 Published online Aug 15, 2025. doi: 10.4239/wjd.v16.i8.108310
Rheb1 as a novel β-cell regulator connecting mTORC1, AMPK, and NOTCH1 pathways for efficient diabetes therapy
Mostafa M Gouda
Mostafa M Gouda, College of Biosystems Engineering and Food Science, Zhejiang University, Hangzhou 310058, Zhejiang Province, China
Mostafa M Gouda, Department of Nutrition & Food Science, National Research Centre, Giza 12622, Egypt
Author contributions: Gouda MM contributed to conceptualization, methodology, literature search, figure building, and original draft writing and revision of this manuscript.
Supported by Zhejiang University Global Partnership Fund, No. BIO-0322023.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for 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: Mostafa M Gouda, PhD, Professor, College of Biosystems Engineering and Food Science, Zhejiang University, No. 866 Yuhangtang Road, Hangzhou 310058, Zhejiang Province, China. mostafa-gouda@zju.edu.cn
Received: April 11, 2025 Revised: May 19, 2025 Accepted: July 14, 2025 Published online: August 15, 2025 Processing time: 125 Days and 16.6 Hours
Core Tip
Core Tip: This editorial emphasizes the critical role of β-cells in diabetes risk, particularly regarding brain dysfunction and ulceration in young individuals, and underscores the need for further investigation. Recent studies, including that of Yang et al, demonstrate the key influence of Ras homolog enriched in brain 1 on β-cell function and proliferation, which is linked to insulin secretion and glucose levels. This suggests that Ras homolog enriched in brain 1 influences the mammalian target of rapamycin complex 1 and AMP-activated protein kinase pathways, confirming the existence of the islet reflex instead of relying solely on one pathway. This metabolic role opens up therapeutic avenues for advanced treatment targets of diabetes-related brain dysfunction.
