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World J Diabetes. Jul 10, 2015; 6(7): 978-982
Published online Jul 10, 2015. doi: 10.4239/wjd.v6.i7.978
Serum hepcidin concentrations and type 2 diabetes
Alex Aregbesola, Sari Voutilainen, Jyrki K Virtanen, Adeola Aregbesola, Tomi-Pekka Tuomainen
Alex Aregbesola, Sari Voutilainen, Jyrki K Virtanen, Adeola Aregbesola, Tomi-Pekka Tuomainen, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Yliopistonranta 1C, FI70211 Kuopio, Finland
Author contributions: All authors contributed equally to this work.
Conflict-of-interest statement: None declared.
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: Alex Aregbesola, MD, MScPH, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Yliopistonranta 1C, PO Box 1627, FI70211 Kuopio, Finland. alex.aregbesola@uef.fi
Telephone: +358-44-9788099 Fax: +358-17-162936
Received: September 13, 2014
Peer-review started: September 14, 2014
First decision: November 14, 2014
Revised: February 18, 2015
Accepted: March 18, 2015
Article in press: March 20, 2015
Published online: July 10, 2015
Processing time: 300 Days and 0.4 Hours
Abstract

Hepcidin is a peptide hormone with both paracrine and endocrine functions that help in maintaining body iron stores. Type 2 diabetes (T2D) is one of the sequelae of excess body iron stores; thus, iron regulatory hormone hepcidin may have a direct or at least an indirect role in the aetiopathogenesis of T2D. Both human and animal studies at molecular and genetic levels have attempted to establish a role for hepcidin in the development of T2D, and a few epidemiologic studies have also showed a link between hepcidin and T2D at population level, but the findings are still inconclusive. Recent data have suggested different pathways in which hepcidin could be associated with T2D with much emphasis on its primary or secondary role in insulin resistance. Some of the suggested pathways are via transcription modulator of hepcidin (STAT3); ferroportin 1 expression on the cells involved in iron transport; transmembrane protease 6 enzyme; and pro-inflammatory cytokines, interleukin (IL)-1, IL-6, tumor necrosis factor-α and IL-10. This review briefly reports the existing evidence on the possible links between hepcidin and T2D and concludes that more data are needed to confirm or refute hepcidin’s role in the development of T2D. Examining this role could provide a further evidence base for iron in the aetiopathogenesis of T2D.

Keywords: Serum hepcidin; Body iron; Diabetes; Type 2 diabetes; Insulin resistance

Core tip: Excess body iron has been demonstrated as an independent risk factor of type 2 diabetes (T2D). Lately, manipulation of serum hepcidin concentrations through the use of hepcidin agonist is being suggested in the management of iron overload diseases, of which T2D is one. However, little is known about the role of hepcidin in the development of T2D; hence, the need for a review of the existing evidence linking hepcidin and T2D. We discuss some of the main mechanisms through which hepcidin could be associated with T2D.