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Publication Name World Journal of Diabetes
Manuscript ID 104973
Country China
Category Endocrinology & Metabolism
Manuscript Type Basic Study
Article Title Ras homolog enriched in brain 1 regulates β cell mass and β cell function via mTORC1/AMPK/Notch1 pathways
Manuscript Source Unsolicited Manuscript
All Author List Yan Yang, Wan-Juan Song and Jing-Jing zhang
Funding Agency and Grant Number
Funding Agency Grant Number
National Natural Science Foundation of China 82430029
National Natural Science Foundation of China 82330025
National Natural Science Foundation of China 82370807
National Natural Science Foundation of China 82070807
Leading Talents Program of Hunan Province 2022RC3078
Natural Science Foundation of Hunan Province, China 2021JJ30976
Corresponding Author Jing-Jing zhang, MD, PhD, National Clinical Research Center for Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Renmin middle road, Changsha 410011, Hunan Province, China. doctorzhangjj@csu.edu.cn
Key Words Rheb1; β cells; Diabetes; mTOR; AMP-activated protein kinase; Hepatocyte nuclear factor4-alpha
Core Tip Mechanisms underlying β cell dysfunction in diabetes remains unclear, our study explores the role of Ras homolog enriched in brain 1 (Rheb1) in regulating β-cell function and proliferation. The researchers found that Rheb1 is more highly expressed in islets from younger individuals (under 18) compared to adults. Rheb1 promotes β-cell proliferation through both the mTORC1 and AMP-activated protein kinase pathways, rather than relying solely on mTORC1. Moreover, Rheb1 also upregulated key transcription factor HNF4α in β cells. These findings suggest that Rheb1 plays a vital role in β-cell growth and function, making it a promising target for diabetes therapy.
Citation <p>Yang Y, Song WJ, zhang JJ. Ras homolog enriched in brain 1 regulates β cell mass and β cell function via mTORC1/AMPK/Notch1 pathways. <i>World J Diabetes</i> 2025; 16(6): 104973</p>
Received
2025-01-10 10:29
Peer-Review Started
2025-01-13 00:57
To Make the First Decision
Return for Revision
2025-02-11 07:41
Revised
2025-02-19 11:56
Second Decision
2025-03-17 07:06
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief
2025-04-03 07:25
Articles in Press
2025-04-03 07:25
Publication Fee Transferred
2025-02-26 05:20
Edit the Manuscript by Language Editor
Typeset the Manuscript
2025-05-27 02:50
ISSN 1948-9358 (online)
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/
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