Gene expression of divalent metal transporter 1 and transferrin receptor in duodenum of Belgrade rats

Phillip Oates, C. Thomas, E. Freitas, M.J. Callow, Evan Morgan

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Regulation of iron absorption is thought to be mediated by the amount of iron taken up by duodenal crypt cells via the transferrin receptor (TfR)-transferrin cycle and the activity of the divalent metal transporter (DMT1), although DMT1 cannot be detected morphologically in crypt cells. We investigated the uptake of transferrin-bound iron by duodenal enterocytes in Wistar rats fed different levels of iron and Belgrade (b/b) rats in which iron uptake by the transferrin cycle is defective because of a mutation in DMT1. We showed that DMT1 in our colony of b/b rats contains the G185R mutation, which in enterocytes results in reduced cellular iron content and increased DMT1 gene expression similar to levels in iron deficiency of normal rats. In all groups the uptake of transferrin-bound iron by crypt cells was directly proportional to plasma iron concentration, being highest in iron-loaded Wistar rats and b/b rats. We conclude that the uptake of transferrin-bound iron by developing enterocytes is largely independent of DMT1.
Original languageEnglish
Pages (from-to)G930-G936
JournalAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
Volume278
Publication statusPublished - 2000

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Transferrin Receptors
Duodenum
Iron
Gene Expression
Transferrin
Enterocytes
Wistar Rats
solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2
Activity Cycles
Mutation
Metals

Cite this

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title = "Gene expression of divalent metal transporter 1 and transferrin receptor in duodenum of Belgrade rats",
abstract = "Regulation of iron absorption is thought to be mediated by the amount of iron taken up by duodenal crypt cells via the transferrin receptor (TfR)-transferrin cycle and the activity of the divalent metal transporter (DMT1), although DMT1 cannot be detected morphologically in crypt cells. We investigated the uptake of transferrin-bound iron by duodenal enterocytes in Wistar rats fed different levels of iron and Belgrade (b/b) rats in which iron uptake by the transferrin cycle is defective because of a mutation in DMT1. We showed that DMT1 in our colony of b/b rats contains the G185R mutation, which in enterocytes results in reduced cellular iron content and increased DMT1 gene expression similar to levels in iron deficiency of normal rats. In all groups the uptake of transferrin-bound iron by crypt cells was directly proportional to plasma iron concentration, being highest in iron-loaded Wistar rats and b/b rats. We conclude that the uptake of transferrin-bound iron by developing enterocytes is largely independent of DMT1.",
author = "Phillip Oates and C. Thomas and E. Freitas and M.J. Callow and Evan Morgan",
year = "2000",
language = "English",
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journal = "American journal of of physiology : gastrointestinal and liver physiology",
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publisher = "American Physiological Society",

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Gene expression of divalent metal transporter 1 and transferrin receptor in duodenum of Belgrade rats. / Oates, Phillip; Thomas, C.; Freitas, E.; Callow, M.J.; Morgan, Evan.

In: American Journal of Physiology-Gastrointestinal and Liver Physiology, Vol. 278, 2000, p. G930-G936.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Gene expression of divalent metal transporter 1 and transferrin receptor in duodenum of Belgrade rats

AU - Oates, Phillip

AU - Thomas, C.

AU - Freitas, E.

AU - Callow, M.J.

AU - Morgan, Evan

PY - 2000

Y1 - 2000

N2 - Regulation of iron absorption is thought to be mediated by the amount of iron taken up by duodenal crypt cells via the transferrin receptor (TfR)-transferrin cycle and the activity of the divalent metal transporter (DMT1), although DMT1 cannot be detected morphologically in crypt cells. We investigated the uptake of transferrin-bound iron by duodenal enterocytes in Wistar rats fed different levels of iron and Belgrade (b/b) rats in which iron uptake by the transferrin cycle is defective because of a mutation in DMT1. We showed that DMT1 in our colony of b/b rats contains the G185R mutation, which in enterocytes results in reduced cellular iron content and increased DMT1 gene expression similar to levels in iron deficiency of normal rats. In all groups the uptake of transferrin-bound iron by crypt cells was directly proportional to plasma iron concentration, being highest in iron-loaded Wistar rats and b/b rats. We conclude that the uptake of transferrin-bound iron by developing enterocytes is largely independent of DMT1.

AB - Regulation of iron absorption is thought to be mediated by the amount of iron taken up by duodenal crypt cells via the transferrin receptor (TfR)-transferrin cycle and the activity of the divalent metal transporter (DMT1), although DMT1 cannot be detected morphologically in crypt cells. We investigated the uptake of transferrin-bound iron by duodenal enterocytes in Wistar rats fed different levels of iron and Belgrade (b/b) rats in which iron uptake by the transferrin cycle is defective because of a mutation in DMT1. We showed that DMT1 in our colony of b/b rats contains the G185R mutation, which in enterocytes results in reduced cellular iron content and increased DMT1 gene expression similar to levels in iron deficiency of normal rats. In all groups the uptake of transferrin-bound iron by crypt cells was directly proportional to plasma iron concentration, being highest in iron-loaded Wistar rats and b/b rats. We conclude that the uptake of transferrin-bound iron by developing enterocytes is largely independent of DMT1.

M3 - Article

VL - 278

SP - G930-G936

JO - American journal of of physiology : gastrointestinal and liver physiology

JF - American journal of of physiology : gastrointestinal and liver physiology

SN - 0193-1857

ER -