摘要
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 T2 D.Both human and animal studies at molecular and genetic levels have attemptedto establish a role for hepcidin in the development of T2 D,and a few epidemiologic studies have also showed a link between hepcidin and T2 D at population level,but the findings are still inconclusive.Recent data have suggested different pathways in which hepcidin could be associated with T2 D 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 T2 D and concludes that more data are needed to confirm or refute hepcidin's role in the development of T2 D.Examining this role could provide a further evidence base for iron in the aetiopathogenesis of T2 D.
Hepcidin is a peptide hormone with both paracrine andendocrine functions that help in maintaining body ironstores. Type 2 diabetes （T2D） is one of the sequelae ofexcess body iron stores; thus, iron regulatory hormonehepcidin may have a direct or at least an indirect role inthe aetiopathogenesis of T2D. Both human and animalstudies at molecular and genetic levels have attemptedto establish a role for hepcidin in the development ofT2D, and a few epidemiologic studies have also showeda link between hepcidin and T2D at population level,but the findings are still inconclusive. Recent data havesuggested different pathways in which hepcidin could beassociated with T2D with much emphasis on its primaryor secondary role in insulin resistance. Some of thesuggested pathways are via transcription modulator ofhepcidin （STAT3）; ferroportin 1 expression on the cellsinvolved in iron transport; transmembrane protease 6enzyme; and pro-inflammatory cytokines, interleukin（IL）-1, IL-6, tumor necrosis factor-α and IL-10. Thisreview briefly reports the existing evidence on thepossible links between hepcidin and T2D and concludesthat more data are needed to confirm or refute hepcidin＇srole in the development of T2D. Examining this rolecould provide a further evidence base for iron in theaetiopathogenesis of T2D.
