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Effect of nicotine exposure on cellular and molecular parameters of vitamin B1 (thiamin) uptake by pancreatic acinar cells (896.3)
Author(s) -
Srinivasan Padmanabhan,
Subramanian Veedamali,
Kapadia Sameer,
Said Hamid
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.896.3
Subject(s) - nicotine , endocrinology , in vivo , in vitro , medicine , messenger rna , chemistry , biology , gene , biochemistry , microbiology and biotechnology
Pancreatic acinar cells take in thiamin by a specific carrier‐mediated process that involve both THTR‐1 and THTR‐2 (encoded by SLC19A2 and SLC19A3, respectively). In this study we examined the effect of chronic exposure of mouse pancreatic acinar in vivo (wild‐type and transgenic mice carrying the SLC19A2 and SLC19A3 promoters) and human pancreatic acinar cells in vitro to the cigarette smoke component nicotine on physiological and molecular parameters of the thiamin uptake process. Chronic exposure of mice to nicotine (0.77 mM nicotine in drinking water for 4 wks) leads to a significant decrease in thiamin uptake, expression of THTR‐1 and ‐2 protein, mRNA levels and activity of the SLC19A2 and SLC19A3 promoters expressed in transgenic mice. A decrease in the level of expression of protein and mRNA of the thiamin‐metabolizing enzymes TPKase and thiamin pyrophosphatase (TPPase) was observed. Similarly chronic exposure of human pancreatic acinar cells to nicotine (0.5 µM, 48 h) leads to a significant inhibition in thiamin uptake, as well as in the level of expression of THTR‐1 and ‐2 protein and mRNA. These results demonstrate, for the first time, that chronic exposure of pancreatic acinar cells to nicotine negatively impacts the physiological and molecular parameters of thiamin uptake and that this effect is exerted, at least in part, at the level of transcription of the SLC19A2 and SLC19A3 genes. Grant Funding Source : Supported by NIH grants AA 018071 and DK‐56061