ORIGINAL RESEARCH article
Front. Aging
Sec. Musculoskeletal Aging
Volume 6 - 2025 | doi: 10.3389/fragi.2025.1564730
This article is part of the Research TopicExploring the Interplay of Aging, Obesity, and Oral Health in Elderly PopulationsView all 4 articles
EI24 binds to IGF1R, enhancing glucose homeostasis and fostering healthy aging in male mice
Provisionally accepted
You-Min Kim1
Seung Eon Lee1Yaechan Song1Tae Wook Nam2Jaehoon Lee1,2
Je Kyung Seong3,4
Wan Namkung5*Han-Woong Lee1,2*- 1Yonsei University, Seoul, Republic of Korea
- 2GEMCRO, Inc, Seoul, Republic of Korea
- 3Korea Model animal Priority Center (KMPC), Seoul National University, Seoul, Republic of Korea
- 4Laboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea
- 5College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Seoul, Republic of Korea
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Introduction: The etoposide-induced 2.4 kb transcript (EI24) plays a crucial role in autophagy, facilitating the clearance of damaged proteins and organelles to maintain cellular homeostasis. While autophagy is widely recognized for its beneficial effects on healthy aging, the effects of EI24 overexpression remain unclear. Methods: We analyzed the interaction of EI24 with the insulin-like growth factor 1 receptor (IGF1R), a key molecule associated with aging. Ei24 transgenic (TG) mice were generated to assess the effects of Ei24 overexpression on aging, glucose homeostasis, and resistance to streptozotocin (STZ)-induced diabetes. Results: EI24 was found to bind to IGF1R, specifically engaging with its transmembrane (TM) domain near the cytoplasmic membrane, and suppress its phosphorylation. Male Ei24 TG mice exhibited signs of healthier aging, with reduced aging markers in the kidney, liver, and pancreas. Moreover, Ei24 overexpression enhanced glucose uptake, likely due to increased Glut4 expression in muscle tissue. Ei24 TG mice also demonstrated resistance to high-dose STZinduced diabetes. Conclusion: These findings suggest that Ei24 overexpression contributes to improved glucose regulation and healthier aging across multiple organs. By interacting with IGF1R, EI24 may provide a novel mechanism for promoting metabolic and age-related health.
Keywords: EI24, Aging, GLUT4, IGF1R, Diabetes Mellitus
Received: 29 Jan 2025; Accepted: 20 May 2025.
Copyright: © 2025 Kim, Lee, Song, Nam, Lee, Seong, Namkung and Lee. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Wan Namkung, College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Seoul, Republic of Korea
Han-Woong Lee, Yonsei University, Seoul, Republic of Korea
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