Wongdee K, Charoenphandhu N. Update on type 2 diabetes-related osteoporosis. World J Diabetes 2015; 6(5): 673-678 [PMID: 26069716 DOI: 10.4239/wjd.v6.i5.673]
Corresponding Author of This Article
Narattaphol Charoenphandhu, MD, PhD, Department of Physiology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok 10400, Thailand. naratt@narattsys.com
Research Domain of This Article
Endocrinology & Metabolism
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. Jun 10, 2015; 6(5): 673-678 Published online Jun 10, 2015. doi: 10.4239/wjd.v6.i5.673
Update on type 2 diabetes-related osteoporosis
Kannikar Wongdee, Narattaphol Charoenphandhu
Kannikar Wongdee, Narattaphol Charoenphandhu, Center of Calcium and Bone Research (COCAB), Faculty of Science, Mahidol University, Bangkok 10400, Thailand
Kannikar Wongdee, Office of Academic Management, Faculty of Allied Health Sciences, Burapha University, Chonburi 20131, Thailand
Narattaphol Charoenphandhu, Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand
Author contributions: Wongdee K and Charoenphandhu N contributed equally for literature review, data analysis and preparation of the manuscript.
Supported by Grants from the Cluster and Program Management Office (CPMO), National Science and Technology Development Agency (P-11-00639); the Thailand Research Fund (TRF)-Mahidol University through the TRF Senior Research Scholar Grant (RTA5780001 to NC); the Faculty of Allied Health Sciences, Burapha University and Thailand Research Fund through TRF Research Career Development Grant (RSA5780041 to KW); the Research and Development Fund Burapha University (05/2557 to KW); the Faculty of Allied Health Sciences, Burapha University Research Grant of Fiscal Year 2015 (AHS05/2558 to KW).
Conflict-of-interest: Kannikar Wongdee and Narattaphol Charoenphandhu declare no conflicts of interest.
Open-Access: 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/
Correspondence to: Narattaphol Charoenphandhu, MD, PhD, Department of Physiology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok 10400, Thailand. naratt@narattsys.com
Telephone: +66-2-3547154 Fax: +66-2-3547154
Received: January 11, 2015 Peer-review started: January 15, 2015 First decision: February 7, 2015 Revised: February 12, 2015 Accepted: March 5, 2015 Article in press: March 9, 2015 Published online: June 10, 2015 Processing time: 158 Days and 17.7 Hours
Core Tip
Core tip: Type 2 diabetes mellitus (T2DM) negatively affects bone density and strength by inducing cellular and extracellular matrix failures. Insulin resistance in T2DM deteriorates osteoblast proliferation and activity, but enhances osteoclast activity, leading to uncoupled bone remodeling. Hyperglycemia also aggravates osteoblast dysfunction, thus contributing to cellular failure. Extracellular matrix failure is caused by abnormal collagen synthesis and aberrant collagen structure and alignment, the latter of which results, in part, from advanced glycation end products (AGEs). With hyperglycemia and AGEs, impaired bone strength may occur despite high bone mineral density. It is, therefore, concluded that T2DM can be considered a cause of osteoporosis and/or poor bone mechanical properties.
