In:
European Journal of Endocrinology, Oxford University Press (OUP), Vol. 173, No. 5 ( 2015-11), p. 643-653
Abstract:
Iron has been suggested to play a role in the etiology of type 2 diabetes mellitus (T2DM). Except for ferritin, evidence is sparse for other markers of iron metabolism that are regulated differently and might act through independent pathways. We therefore investigated the associations of serum ferritin, transferrin, soluble transferrin receptor (sTfR), transferrin saturation (TSAT), sTfR-to-log 10 ferritin (sTfR-F) index, and iron with impaired glucose metabolism (IGM/‘prediabetes’), T2DM, and four continuous glucose and insulin traits. Design and methods Data from 2893 participants of the population-based Cooperative Health Research in the Region of Augsburg (KORA) F4 study (Germany) was investigated through regression analysis. The results were adjusted for socio-demographic, life-style, and obesity measures as well as metabolic, inflammatory, and other iron biomarkers following a step-wise approach. Non-linearity was tested by adding a non-linear spline component to the model. Results Ferritin and transferrin were positively associated with IGM (fourth vs first sex-specific quartile: ferritin odds ratio (OR)=2.08 (95% CI 1.43–3.04) and transferrin OR=1.89 (95% CI 1.32–2.70)), T2DM (ferritin OR=1.98 (95% CI 1.22–3.22) and transferrin OR=2.42 (95% CI 1.54–3.81)), and fasting as well as 2-h glucose. TSAT (OR=0.55 (95% CI 0.34–0.88)) and iron (OR=0.61 (95% CI 0.38–0.97)) were inversely associated with T2DM, sTfR-F-index was inversely associated with IGM (OR=0.67 (95% CI 0.48–0.95)). There was no strong evidence for non-linear relationships. Conclusions The observed associations of several markers of iron metabolism with hyperglycemia and insulin resistance suggest that iron stores as well as iron-related metabolic pathways contribute to the pathogenesis of IGM and T2DM. Moreover, TSAT levels are decreased in T2DM patients.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
2015
detail.hit.zdb_id:
1485160-X
