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Iron deficiency and anaemia: Blame it on intestinal cells that don't let iron enter blood

Fatigue and weakness? One study result has implicated certain intestinal immune cells in the absorption of iron, leading to its inability to enter the bloodstream and causing iron deficiency

April 21, 2023 / 15:03 IST
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Iron plays a critical role in our body. An important component of the blood pigment haemoglobin, it is responsible for transporting oxygen in the red blood cells, a lack of which causes anaemia. According to the World Health Organisation, more than 1.60 billion people all over the world are anaemic, meaning they are affected by iron deficiency. Fatigue and weakness, pale skin, shortness of breath, dizziness, headaches, cold hands and feet, and a weakened immune system are some of the symptoms of iron deficiency.

Researchers have now found evidence that implicates certain intestinal immune cells in the absorption of iron, resulting in its inability to enter the bloodstream and causing iron deficiency in the body. The researchers from MedUni Vienna, Austria, have shown that certain immune cells called macrophages control iron absorption in the intestine’s duodenum, where one to two milligrams of iron, a trace element, need to be absorbed for a balanced iron metabolism.

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Their study results, published in the journal Blood, could provide therapeutic measures to address iron deficiency, is one of the five main causes of impaired health and affects 30 percent of the world’s population, particularly women. The research revealed that activation of macrophages directly in the duodenum leads to a halt in iron availability in the body.

"We were able to determine that the macrophages in the duodenum eat away the iron transport molecule transferrin, so to speak. This means that the iron remains in the intestinal cells and can no longer enter the bloodstream,” explained first author Nyamdelger Sukhbaatar from MedUni Vienna. The study also found that macrophages are also activated during fasting, food intake or during an intestinal infection, thereby changing the amount of transferrin in the intestine. "Our findings thus represent a real paradigm shift, as it was previously assumed that transferrin is always present in equal amounts everywhere in the body and does not actually play any role in iron regulation,” underlined study leader Thomas Weichhart.