Abstract

Summary. The sla mouse has a hereditary iron deficiency anaemia and inappropriately low absorption of dietary iron. The response of the iron transport system in sla to a variety of factors that stimulate iron absorption in the normal mouse was investigated. The administration of an iron deficient diet for 5 days significantly increased the absorption of iron from graded oral doses of 59Fe ascorbate in both sla and normal mice compared with control groups fed an iron supplemented diet. Curvilinear dose‐absorption relationships indicated a saturable component in the iron transport system of both sla and normal mice fed the iron deficient diet. This suggests that the actual transport process is intact and can be activated by dietary iron deprivation. Phenobarbital enhanced the response to an iron deficient diet in both normal and sla but had no effect in animals given an iron containing semi‐synthetic diet. Blood loss, erythropoietin and hypoxia did not affect iron absorption in sla mice fed an iron supplemented cube diet, in contrast to a marked increase in normal mice. It appears that the iron transport pathway in sla mice has a limited capacity when saturated with dietary iron, but normal regulatory mechanisms operate when the pathway is not saturated. Whether the primary defect lies in a mucosal intracellular component or in an extracellular stimulus to activate iron transport is not clear.

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