RGD Reference Report - Effect of chronic kidney disease on the expression of thiamin and folic acid transporters. - Rat Genome Database

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Effect of chronic kidney disease on the expression of thiamin and folic acid transporters.

Authors: Bukhari, FJ  Moradi, H  Gollapudi, P  Ju Kim, H  Vaziri, ND  Said, HM 
Citation: Bukhari FJ, etal., Nephrol Dial Transplant. 2011 Jul;26(7):2137-44. doi: 10.1093/ndt/gfq675. Epub 2010 Dec 13.
RGD ID: 7327184
Pubmed: PMID:21149507   (View Abstract at PubMed)
PMCID: PMC3164444   (View Article at PubMed Central)
DOI: DOI:10.1093/ndt/gfq675   (Journal Full-text)

BACKGROUND: Chronic kidney disease (CKD) is associated with significant cardiovascular, neurological and metabolic complications. Thiamin and folate are essential for growth, development and normal cellular function, and their uptake is mediated by regulated transport systems. While plasma folate and thiamin levels are generally normal in patients with CKD, they commonly exhibit features resembling vitamin deficiency states. Earlier studies have documented impaired intestinal absorption of several B vitamins in experimental CKD. In this study, we explored the effect of CKD on expression of folate and thiamin transporters in the key organs and tissues. METHODS: Sprague-Dawley rats were randomized to undergo 5/6 nephrectomy or sham operation and observed for 12 weeks. Plasma folate and thiamin concentrations and gene expression of folate (RFC, PCFT) and thiamin transporters (THTR-1 and THTR-2) were determined in the liver, brain, heart and intestinal tissues using real-time PCR. Hepatic protein abundance of these transporters was determined using western blot analysis. RESULTS: Plasma folate and thiamin levels were similar between the CKD and the control groups. However, expressions of both folate (RFC and PCFT) and thiamin (THTR-1, THTR-2) transporters were markedly reduced in the small intestine, heart, liver and brain of the CKD animals. Liver protein abundance of folate and thiamin transporters was significantly reduced in the CKD animals when compared with the sham-operated controls. Furthermore, we found a significant reduction in mitochondrial folate and thiamin transporters in the CKD animals. CONCLUSIONS: CKD results in marked down-regulation in the expression of folate and thiamin transporters in the intestine, heart, liver and brain. These events can lead to reduced intestinal absorption and impaired cellular homeostasis of these essential micronutrients despite their normal plasma levels.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
chronic kidney disease  ISOSlc19a1 (Rattus norvegicus)7327184; 7327184mRNA:decreased expression:multiple (rat)RGD 
chronic kidney disease  ISOSlc19a2 (Rattus norvegicus)7327184; 7327184mRNA:decreased expression:liver and heart (rat)RGD 
chronic kidney disease  ISOSlc19a3 (Rattus norvegicus)7327184; 7327184mRNA:decreased expression:liver more ...RGD 
chronic kidney disease  ISOSlc46a1 (Rattus norvegicus)7327184; 7327184mRNA:decreased expression:liver more ...RGD 
chronic kidney disease  IEP 7327184mRNA:decreased expression:multiple (rat)RGD 
chronic kidney disease  IEP 7327184mRNA:decreased expression:liver and heart (rat)RGD 
chronic kidney disease  IEP 7327184; 7327184mRNA:decreased expression:liver more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Slc19a1  (solute carrier family 19 member 1)
Slc19a2  (solute carrier family 19 member 2)
Slc19a3  (solute carrier family 19 member 3)
Slc46a1  (solute carrier family 46 member 1)

Genes (Mus musculus)
Slc19a1  (solute carrier family 19 (folate transporter), member 1)
Slc19a2  (solute carrier family 19 (thiamine transporter), member 2)
Slc19a3  (solute carrier family 19, member 3)
Slc46a1  (solute carrier family 46, member 1)

Genes (Homo sapiens)
SLC19A1  (solute carrier family 19 member 1)
SLC19A2  (solute carrier family 19 member 2)
SLC19A3  (solute carrier family 19 member 3)
SLC46A1  (solute carrier family 46 member 1)


Additional Information