{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T17:00:27Z","timestamp":1793293227186,"version":"4.5.0"},"reference-count":0,"publisher":"IMR Press","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["International Journal for Vitamin and Nutrition Research"],"published-print":{"date-parts":[[2013,6,1]]},"abstract":"<jats:p> It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1\u03b1) transcription factor, resulting in the trans-activation of HIF-1\u03b1 regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1\u03b1 stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1\u03b1 stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1\u03b1-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency. <\/jats:p>","DOI":"10.1024\/0300-9831\/a000159","type":"journal-article","created":{"date-parts":[[2014,5,21]],"date-time":"2014-05-21T01:39:47Z","timestamp":1400636387000},"page":"188-197","source":"Crossref","is-referenced-by-count":33,"title":["HIF1-\u03b1-Mediated Gene Expression Induced by Vitamin B<sub>1<\/sub> Deficiency"],"prefix":"10.31083","volume":"83","author":[{"given":"Rebecca L.","family":"Sweet","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason A.","family":"Zastre","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"16242","container-title":["International Journal for Vitamin and Nutrition Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/econtent.hogrefe.com\/doi\/pdf\/10.1024\/0300-9831\/a000159","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,8,9]],"date-time":"2024-08-09T02:09:41Z","timestamp":1723169381000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.imrpress.com\/journal\/IJVNR\/83\/3\/10.1024\/0300-9831\/a000159"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2013,6,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,6,1]]}},"alternative-id":["10.1024\/0300-9831\/a000159"],"URL":"https:\/\/doi.org\/10.1024\/0300-9831\/a000159","relation":{},"ISSN":["0300-9831","1664-2821"],"issn-type":[{"value":"0300-9831","type":"print"},{"value":"1664-2821","type":"electronic"}],"subject":[],"published":{"date-parts":[[2013,6,1]]}}}