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9/22/2025 5:23:54 AM | Browse: 20 | Download: 0
Publication Name World Journal of Diabetes
Manuscript ID 112236
Country China
Category Endocrinology & Metabolism
Manuscript Type Review
Article Title Androgen receptor mutations in familial androgen insensitivity syndrome: A metabolic reprogramming pathway to type 2 diabetes susceptibility
Manuscript Source Invited Manuscript
All Author List Cheng Luo, Wei-Wei Zhang, Liang-Yan Hua, Mei-Qi Zeng, Hui Xu, Cheng-Zheng Duan, Shi-Yu Xu, Shuo Zhan, Xiao-Fei Pan, Da Sun, Li-Ya Ye and Dong-Juan He
Funding Agency and Grant Number
Funding Agency Grant Number
Quzhou Science and Technology Plan Project No. 2022K69
Corresponding Author Dong-Juan He, Chief Physician, Dean, Director, Professor, Department of Endocrinology, The Second People’s Hospital of Quzhou, No. 338 Xin’an Avenue, Qujiang District, Quzhou 324002, Zhejiang Province, China. hedongjuan1247@wmu.edu.cn
Key Words Androgen insensitivity syndrome; Androgen receptor; Gene mutation; Metabolic reprogramming; Type 2 diabetes
Core Tip Familial androgen insensitivity syndrome (AIS), caused by androgen receptor gene mutations, has long been viewed as a disorder of sex development. However, recent findings revealed that androgen receptor dysfunction also drives metabolic reprogramming in key tissues - pancreatic β-cells, skeletal muscle, liver, and adipose tissue - leading to insulin resistance and increased susceptibility to type 2 diabetes mellitus. This article highlights emerging evidence of glucagon-like peptide-1 signaling disruption, mitochondrial dysfunction, and inflammatory imbalance in AIS. We propose an integrated framework of genetic screening, endocrine surveillance, and individualized therapy to improve long-term metabolic outcomes and prevent cardiometabolic complications in AIS patients.
Citation Luo C, Zhang WW, Hua LY, Zeng MQ, Xu H, Duan CZ, Xu SY, Zhan S, Pan XF, Sun D, Ye LY, He DJ. Androgen receptor mutations in familial androgen insensitivity syndrome: A metabolic reprogramming pathway to type 2 diabetes susceptibility. World J Diabetes 2025; In press
Received
2025-07-22 03:31
Peer-Review Started
2025-07-24 00:11
To Make the First Decision
Return for Revision
2025-08-06 11:08
Revised
2025-08-06 16:46
Second Decision
2025-09-08 00:16
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief
2025-09-22 05:23
Articles in Press
2025-09-22 05:23
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
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: http://creativecommons.org/Licenses/by-nc/4.0/
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