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Increased Small Intestine Expression of Non‐Heme Iron Transporters in Morbidly Obese Patients With Newly Diagnosed Type 2 Diabetes
Author(s) -
MorenoNavarrete José María,
Rodríguez Amaia,
Becerril Sara,
Valentí Víctor,
Salvador Javier,
Frühbeck Gema,
FernándezReal José Manuel
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700301
Subject(s) - hepcidin , medicine , ferritin , type 2 diabetes , ferroportin , endocrinology , small intestine , diabetes mellitus , hmox1 , hemochromatosis , chemistry , heme , biochemistry , heme oxygenase , anemia , enzyme
Scope To investigate intestinal markers of iron absorption in morbidly obese subjects according to glucose tolerance. Methods and results Gene expression of both non‐heme ( SLC40A1 (ferroportin) , SLC11A2 ) and heme iron ( SLC46A1 (HCP1), HMOX1 ) transporters is analyzed in 38 small intestine tissue samples [11 with normal glucose tolerance, 14 with glucose intolerance (GI), and 13 with newly diagnosed type 2 diabetes (T2D)]. SLC40A1 ( r = 0.43, p = 0.008) and SLC11A2 ( r = 0.35, p = 0.03) mRNA levels are positively correlated with ferritin‐to‐hepcidin ratio and with fasting glucose, being significantly increased in patients with T2D. Only ferroportin is negatively associated with serum hepcidin ( r = –0.617, p < 0.0001). In multivariate regression analysis, fasting glucose contributes independently to intestinal SLC40A1 ( p = 0.009) and SLC11A2 ( p = 0.04) variance after controlling for age, sex, and BMI. When circulating hepcidin is incorporated into the model, fasting glucose contributes significantly and independently to intestinal SLC40A1 ( p = 0.02), but not to SLC11A2 ( p = 0.07) variance. SLC46A1 and HMOX1 are similar in all groups. Conclusion The expression of ferroportin and SLC11A2 is increased in the intestine of patients with T2D in association with iron stores and serum hepcidin levels. Increased intestinal iron absorption is a potential mechanism that could explain the increased body iron stores frequently observed in patients with T2D.