A comparison of cobalamin binding by liver and kidney in rat and man

Scott, J. S. D.; Bowman, Edward P.; Cooksley, W. G. E.

doi:10.1042/cs0680357

Cited by 5 publications

(1 citation statement)

References 20 publications

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“…This suggestion may help explain why in the rat most of the absorbed Cbl is retained in the kidney [30]. In support of these observations are studies [31,32] that have suggested that in the rat, the kidney acts as a storage site for Cbl. The high levels of TC II-R expression in the intestine may help in facilitating the Cbl needs of rapidly proliferating enterocytes along the entire horizontal axis of the gut.…”

Section: Resultsmentioning

confidence: 79%

Regulation of expression of transcobalamin II receptor in the rat

Bose

Seetharam

Hammond

et al. 1995

Biochemical Journal

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Surface and intracellular membrane distribution and hormonal regulation of transcobalamin II receptor (TC II-R) activity and protein levels have been studied in an effort to understand its regulation of expression in the rat. TC II-R activity and the levels of the 62 kDa monomeric and 124 kDa dimeric forms of TC II-R were highest in the rat kidney and intestine, and in these tissues the receptor expression was not dependent upon the postnatal development of the rat. TC II-R expression was uniform in the various regions of the gut. Surface membrane distribution of TC II-R in the kidney revealed the expression of the 124 kDa dimer form of TC II-R in the apical and basolateral membranes in the ratio of 1:10. Further subcellular distribution of TC II-R in the kidney revealed the expression of the 124 kDa dimer in the intermicrovillar clefts and clathrin-coated vesicles and the 62 kDa monomer in the microsomes. Neither the monomer nor the dimer could be detected in the early endosomes or lysosomes. Membrane TC II-R activity and TC II-R protein levels and cobalamin (Cbl; vitamin B12) transport in vivo were inhibited by about 90% in adrenalectomized rats and all three returned to normal levels by oral treatment of these animals with cortisone acetate. In contrast, thyroidectomy or experimentally induced diabetes had no effect on TC II-R activity or Cbl transport. Based on these observations, we suggest that TC II-R expression is not developmentally or regionally regulated in rat renal and intestinal membranes and its expression in the kidney is asymmetrically distributed between the apical (10%) and basolateral (90%) membranes. In addition, our results also show that the dimerization of TC II-R is a post-microsomal event and that the expression of TC II-R and plasma Cbl transport is regulated by cortisone.

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Section: Resultsmentioning

confidence: 79%