The relationship between iron and glucose metabolism has been evidenced strongly, but the molecular mediation of this connection is just being revealed. The discovery of hepcidin as the prime controller of iron metabolism has paved the way for understanding the main actors behind this mediation. Recent data suggest that insulin therapy and probably other diabetes drugs can influence hepcidin production, thus influencing the iron load in cells. Correcting iron load through hepcidin expression could be a novel and important mechanism of action of antidiabetes drugs. This effect would further establish the protective role of antidiabetes therapy and might even affect prevention strategies in diabetes. In this review, we summarize the recent data about iron-glucose links through hepcidin expression, the molecular mediation of this interplay and the clinical implications of these findings.
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| http://dx.doi.org/10.1016/j.jcjd.2017.04.007 | DOI Listing |
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