Iron Metabolism in Type 2 Diabetes Management

Iron plays a dual role in type 2 diabetes, acting both as an essential cofactor in metabolic pathways and as a potential driver of oxidative stress when in excess. Under normal conditions, iron is absorbed in the duodenum, stored in ferritin complexes and mobilised via ferroportin under the regulation of hepcidin. In pancreatic β-cells, iron supports mitochondrial respiration and ATP production, thereby facilitating insulin synthesis and secretion. However, chronically elevated body iron stores can promote the formation of reactive oxygen species and impair insulin signalling in peripheral tissues. Dysregulation of hepcidin synthesis in insulin-resistant states further exacerbates iron overload, leading to a vicious cycle of oxidative damage, β-cell dysfunction and progressive glucose intolerance. Understanding the hormonal and molecular controls of iron uptake, storage and export has opened new avenues for adjunctive strategies in diabetes care, ranging from dietary modulation of heme iron intake to pharmacological hepcidin mimetics. Integrating iron‐centric biomarkers into routine risk assessment may help to personalise glycaemic management and to prevent long-term vascular complications.

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Iron Metabolism in Type 2 Diabetes Management publication trend

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Technical terms

Ferritin: Intracellular protein complex that stores iron and releases it in a controlled fashion; serum ferritin reflects systemic iron stores.

Hepcidin: Liver‐derived peptide hormone that binds to the iron exporter ferroportin, triggering its degradation and reducing iron efflux from enterocytes and macrophages.

Ferroportin: The sole known cellular iron exporter, expressed on enterocytes, hepatocytes and macrophages; regulated post-translationally by hepcidin.

Reactive oxygen species (ROS): Highly reactive derivatives of oxygen formed during cellular metabolism; excessive ROS induce oxidative damage to lipids, proteins and DNA.

β-cell: Insulin‐producing cell in the pancreatic islets of Langerhans; requires precise iron homeostasis for mitochondrial ATP generation and regulated insulin release.

Transferrin saturation: The percentage of transferrin binding sites occupied by iron; an indicator of circulating iron availability and potential oxidative risk.

References

1. Nutritional Aspects of Iron in Health and Disease. Nutrients (2023).
2. Body Iron Stores and Heme-Iron Intake in Relation to Risk of Type 2 Diabetes: A Systematic Review and Meta-Analysis. PLOS ONE (2012).
3. Hepcidin levels in diabetes mellitus and polycystic ovary syndrome. Diabetic Medicine (2013).
4. Elevated Serum Ferritin Level Is Associated with the Incident Type 2 Diabetes in Healthy Korean Men: A 4 Year Longitudinal Study. PLOS ONE (2013).
5. Iron Metabolism in Pancreatic Beta-Cell Function and Dysfunction. Cells (2021).