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Defeat Diabetes Foundation

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Diabetes Cause Linked to Iron

Posted: Monday, October 01, 2012

The pancreas is the "diabetes organ" because it produces beta cells, found in the islets of Langerhans, which play a crucial role in the disease. Beta cells respond to an increase in sugar levels in the blood stream by releasing insulin (which they store) and also producing more of the hormone so sugar can be transported into the cells.

In people who have type 2 diabetes, the beta cells are unable to produce enough of the insulin the body needs. One reason for this problem may be blamed on the increased activity of a protein that transports iron and also destroys beta cells.

According to Professor Thomas Mandrup-Poulsen, of the Department of Biomedical Sciences, "increased activity of a certain iron transporter causes damage to the beta cell," which can lead to diabetes. More specifically, in this new study, which was conducted using mice, the researchers reported several important findings:

It is the first study to show a link between inflammation and the transport of iron, which the investigators believe to be the underlying cause of a higher risk for diabetes;
Inflammatory signal factors produced around the beta cells in people who have either type 1 or type 2 diabetes speed up the activity of the iron transporter; and
Removal of the iron transporter in genetically modified mice resulted in the animals being protected against diabetes.

A recent (2012) meta-analysis published in PLoS One explored the relationship between the body's iron stores or iron intake from the diet and the risk of type 2 diabetes. Sixteen studies were evaluated with a total of more than 13,500 patients with type 2 diabetes and more than 220,000 controls. The final review also included an additional 15 studies.

Overall, the reviewers found that increased levels of stored iron and iron intake from the diet were both associated with a higher risk of type 2 diabetes.

In the October 2011 issue of Diabetes Care, researchers noted the effect of elevated transferrin saturation on the risk of diabetes. Transferrin is a type of glycoprotein that binds with iron and controls the amount of free iron in the blood.

The researchers combined patient information from three population-type studies, giving them a total of 8,535 patients with diabetes and 37,039 controls. Overall they found that elevated transferrin saturation was associated with a two- to three-fold increase risk of developing type 1 diabetes or type 2 diabetes.

In a prior study published in Diabetes Care, a research team looked at the role of iron in diabetes and its complications. They noted that both animal and human studies indicate iron plays a part in diabetic nephropathy (kidney disease), atherosclerosis, and vascular disease.

What this new study means is that individuals who have prediabetes or who are concerned about developing diabetes may want to talk to their healthcare providers about their use of iron supplements and iron in their diet. However, Mandrup-Poulsen noted the need to conduct further studies concerning iron content in the body and diabetes risk, and that, "Only then will we be able to advise people at risk of diabetes not to take iron supplements, or recommend drug treatment to reduce the amount of iron in the body."

The findings of the new study also can be applied to research in a number of areas. Although the investigators revealed a link between diabetes -- specifically beta cells -- and iron, the model can be used to study other cells that are sensitive to iron, such as heart and liver cells.

Source: http://www.diabetesincontrol.com/index.php?option=com_content&view=article&id=13607&catid=53&Itemid=8, Ellervik C et al. Elevated transferrin saturation and risk of diabetes: three population-based studies. Diabetes Care 2011 Oct; 34(10): 2256-58 Swaminathan S et al. The role of iron in diabetes and its complications. Diabetes Care 2007 July; 30(7): 1926-33. Zhao Z et al. Body iron stores and heme-iron intake in relation to risk of type 2 diabetes: a systematic review and meta-analysis. PLoS One 2012; 7(7): e41641.