Wang CR, Tsai HW. Anti- and non-tumor necrosis factor-α-targeted therapies effects on insulin resistance in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. World J Diabetes 2021; 12(3): 238-260 [PMID: 33758645 DOI: 10.4239/wjd.v12.i3.238]
Corresponding Author of This Article
Chrong-Reen Wang, MD, PhD, Professor, Department of Internal Medicine, National Cheng Kung University Hospital, No. 138 Sheng-Li Road, Tainan 70403, Taiwan. wangcr@mail.ncku.edu.tw
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
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. Mar 15, 2021; 12(3): 238-260 Published online Mar 15, 2021. doi: 10.4239/wjd.v12.i3.238
Anti- and non-tumor necrosis factor-α-targeted therapies effects on insulin resistance in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis
Chrong-Reen Wang, Hung-Wen Tsai
Chrong-Reen Wang, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan 70403, Taiwan
Hung-Wen Tsai, Department of Pathology, National Cheng Kung University Hospital, Tainan 70403, Taiwan
Author contributions: Wang CR designed the review and wrote the paper; Wang CR and Tsai HW collected and analyzed the clinical data.
Conflict-of-interest statement: The authors declare that they have 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/
Corresponding author: Chrong-Reen Wang, MD, PhD, Professor, Department of Internal Medicine, National Cheng Kung University Hospital, No. 138 Sheng-Li Road, Tainan 70403, Taiwan. wangcr@mail.ncku.edu.tw
Received: December 21, 2020 Peer-review started: December 21, 2020 First decision: January 7, 2021 Revised: January 7, 2021 Accepted: January 21, 2021 Article in press: January 21, 2021 Published online: March 15, 2021
Core Tip
Core Tip: The crucial mechanism leading to development of diabetes mellitus is the resistance of target cells to insulin, i.e. insulin resistance (IR), indicating the ineffective strength of signaling transduction from the receptor, downstream to the final substrates of insulin action. Autoimmune-mediated arthritis including rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, with the involvement of proinflammatory cytokines like tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β as their central pathogenesis, has been demonstrated to be associated with IR. Anti-TNF-α therapy, IL-1 blockade, IL-6 antagonist, Janus kinase inhibitor and phosphodiesterase type 4 blocker can reduce IR and improve diabetic hyperglycemia in autoimmune-mediated arthritis.
