Identification of Novel Disease-Relevant Genes and Pathways in the Pathogenesis of Type 1 Diabetes: A Potential Defect in Pancreatic Iron Homeostasis

What is it about?

High iron exposure has been linked to the development of type 1 diabetes (T1D), but the mechanisms involved are unclear. Using the non-obese diabetic (NOD) mouse model of T1D, we showed that there may be an inflammation-induced loss of iron homeostasis in the islets during disease development. This leads to the accumulation of iron in beta cells, contributing to oxidative stress and beta cell death. We showed that the severity of NOD disease correlates with dietary iron intake. NOD mice maintained on low iron diets had a lower incidence of hyperglycemia while those maintained on high iron diets had an earlier onset and higher incidence of disease. These data suggest that high iron exposure, through diet, combined with a loss of pancreatic iron homeostasis may exacerbate disease. This mechanism could explain the link seen between high iron exposure and the increased risk for T1D in humans.

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