Iron absorption by hypotransferrinaemic mice

British Journal of Haematology - Tập 78 Số 4 - Trang 565-570 - 1991
Robert J. Simpson1, Martin Lombard2,3, Kishor B. Raja1, Ray Thatcher1, T J Peters1
1Department of Clinical Biochemistry, London
2Liver Unit, King's College School of Medicine and Dentistry, London
3Present address: Department of Medicine, University of Liverpool, P.O. Box 147, Liverpool L69 3BX.

Tóm tắt

Summary Iron absorption rates by homozygous and wild‐type mice from a hypotransferrinaemic mouse colony were examined with in vivo tied‐off duodenal sengments and in vitro incubated duodenal fragments. Enhanced initial rates of mucosal uptake and carcass transfer by homozygotes, compared to wild‐types, were observed. The changes in vivo and in in vitro uptake kinetics resemble changes seen in iron deficient or hypoxic mice, suggesting that the liver iron loading shown by homozygotes is due to a failure of the normal mechanism for regulation of iron absorption. In vivo mucosal uptake and carcass transfer of radioiron showed an inverse correlation with liver non‐haem iron content in homozygous hypotransferrinaemic mice, suggesting that some degree of control of absorption, albeit at markedly reduced sensitivity, can operate in these mice. No correlation between haemoglobin level and iron absorption was observed in homozygous hypotransferrinaemic mice, suggesting that this regulator of iron absorption does not function in these mice. The precise pathogenic mechanism of the enhanced iron absorption in hypotransferrinaemia remains to be determined. Mucosal transferrin levels were found to parallel serum transferrin levels in homozygotes. heterozygotes and wild‐type mice. This supports previous suggestions that mucosal transferrin is derived from plasma transferrin and that the enhancement of iron absorption, by physiological mechanisms, does not require the presence of mucosal transferrin.

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