Iron and the Pathophysiology of Diabetes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10161568/
Annu Rev Physiol. Author manuscript; available in PMC 2023 May 5.
Published in final edited form as:
Annu Rev Physiol. 2023 Feb 10; 85: 339–362.
Published online 2022 Sep 22. doi: 10.1146/annurev-physiol-022522-102832
PMCID: PMC10161568
NIHMSID: NIHMS1889793
PMID: 36137277
Iron and the Pathophysiology of Diabetes
Alexandria V Harrison,1 Felipe Ramos Lorenzo,1,2 and Donald A. McClain1,2
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Abstract
High iron is a risk factor for type 2 diabetes mellitus (T2DM) and affects most of its cardinal features: decreased insulin secretion, insulin resistance, and increased hepatic gluconeogenesis. This is true across the normal range of tissue iron levels and in pathologic iron overload. Because of iron’s central role in metabolic processes (e.g., fuel oxidation) and metabolic regulation (e.g., hypoxia sensing), iron levels participate in determining metabolic rates, gluconeogenesis, fuel choice, insulin action, and adipocyte phenotype. The risk of diabetes related to iron is evident in most or all tissues that determine diabetes phenotypes, with the adipocyte, beta cell, and liver playing central roles. Molecular mechanisms for these effects are diverse, although there may be integrative pathways at play. Elucidating these pathways has implications not only for diabetes prevention and treatment, but also for the pathogenesis of other diseases that are, like T2DM, associated with aging, nutrition, and iron.

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