Hepcidin inhibits the iron export from duodenal cells and liver cells into the plasma and therefore plays a key role in controlling iron homeostasis. In obese patients, elevated cytokine production stimulates hepcidin synthesis, causing iron to be retained as ferritin in e.g. macrophages (functional iron deficiency). In addition, patients often develop iron deficiency after bariatric surgery due to malabsorption, which may cause anaemia and thereby lead to complaints such as fatigue. In these patients, the absorption of iron may be disrupted because the reduction of Fe3+ by g astric a cid i nto F e2+ (the form that is easily absorbed) is not so effective after stomach reduction. Iron absorption is further reduced after malabsorptive interventions as a result of bypassing the duodenum and the proximal part of the small intestine, where the absorption takes place. Oral iron supplements often have little effect after bariatric surgery. Intravenous supplements of iron can restore the iron status rapidly after bariatric surgery, resulting in fewer symptoms such as fatigue.