Thiamine Intestinal Transport and Related Issues: Recent Aspects

Gianguido Rindi1 and Umberto Laforenza
P.S.E.B.M. 2000, Vol 224:246–255]

Abstract. In the intestinal lumen thiamine is in free form and very low concentrations. Absorption takes place primarily in the proximal part of the small intestine by means of a dual mechanism, which is saturable at low (physiological) concentrations and diffusive at higher. Thiamine undergoes intracellular phosphorylation mainly to thiamine pyrophosphate, while at the serosal side only free thiamine is present. Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes.
The entry of thiamine into the enterocyte, as evaluated in brush border membrane vesicles of rat small intestine in the absence of H+ gradient, is Na+- and biotransformation-independent, completely inhibited by thiamine analogs and reduced by ethanol administration and aging.

The transport involves a saturable mechanism at low concentrations of vitamin and simple diffusion at higher.
Outwardly oriented H+ gradients enhance thiamine transport, whose saturable component is a Na+-independent electroneutral uphill process utilizing energy supplied by the H+ gradient, and involving a thiamine/ H+ 1:1 stoichiometric exchange.
(so does this mean the ATP pump?)

The exit of thiamine from the enterocyte, as evaluated in basolateral membrane vesicles, is Na+-dependent, directly coupled to ATP hydrolysis by Na+-K+-ATPase, and inhibited by thiamine analogs. Transport of thiamine by renal brush border membrane vesicles is similar to the intestinal as far as both H+ gradient influence and specificity are concerned. In the erythrocyte thiamine transport is a Na+-independent, electroneutral process yet with two components: saturable, prevailing at low thiamine concentrations, and diffusive at higher.

The saturable (specific) component is missing in patients of the rare disease known as thiamine-responsive megaloblastic anaemia (TRMA), producing a general disturbance of thiamine transport up to thiamine deficiency. The TRMA gene is located in chromosome 1q23.3.

Recently, the thiamine transporter has been cloned: it is a protein of 497 aminoacid residues with high homology with the reduced-folate transporter.

http://dx.doi.org/10.1046/j.1525-1373.2000.22428.x

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Regulation of reduced-folate transporter-1 in retinal pigment epithelial cells by folate
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15875363&dopt=Abstract

high folate levels in blood downregulated the folate transporter(and its asociated mRNA levels)..as expected
"Steady-state levels of Reduced-folate transporter-1 (RFT-1) mRNA and protein(ie the actual RTF transporter) decreased significantly in the presence of excess folate.
CONCLUSIONS: Excess folate levels downregulate RFT-1 in RPE."
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my RBC folate is over high?? without any supps(even with avoidance of added folate ) My Mum's RBC folate is over the top of normal too, not far but always over both of us. For some unknown to me reason we have never had our serum folate measured?..

http://jasn.asnjournals.org/cgi/content/full/14/5/1314

seems to be saying that serum folate is usually normal even if RBC folate is high..and its genetic..as I suspected ..and to do with glutamate something...???

and says no influence on serum folate, B12 or anything else.. so not relevant.. or as as far as known :-no effect of this genetic high red blood cell(RBC) folate
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also see following post(s) ~
http://tealady-health.blog.co.uk/2006/09/09/thiamin_transporters~1111873
edit [Bob]
http://www.journals.uchicago.edu/-AJHG/journal/issues/v77n1/42232/42232.html