ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015
Chronic alcohol exposure affects pancreatic acinar mitochondrial thiamin pyrophosphate uptake: studies with mouse 266-6 cell line and primary cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Effect of IL-1β on pancreatic acinar cells mitochondrial TPP carrier-mediated uptake: inhibition mediated via the intracellular NF-κB signaling pathway.American journal of physiology. Cell physiology · 2025Article
- miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury.International journal of molecular sciences · 2023Review
- Targeting Endoplasmic Reticulum Stress as an Effective Treatment for Alcoholic Pancreatitis.Biomedicines · 2022Review
- Posttranscriptional regulation of thiamin transporter-1 expression by microRNA-200a-3p in pancreatic acinar cells.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- What Do We Currently Know about the Pathophysiology of Alcoholic Pancreatitis: A Brief Review.Visceral medicine · 2020Review
- Pyridoxine and pancreatic acinar cells: transport physiology and effect on gene expression profile.American journal of physiology. Cell physiology · 2019Article
- Molecular mechanisms involved in the adaptive regulation of the colonic thiamin pyrophosphate uptake process.American journal of physiology. Cell physiology · 2017Article
- Impact of prevailing thiamin levels on thiamin pyrophosphate uptake in pancreatic acinar cells: do the shuttle!American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Adaptive regulation of pancreatic acinar mitochondrial thiamin pyrophosphate uptake process: possible involvement of epigenetic mechanism(s).American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Uniting Epidemiology and Experimental Disease Models for Alcohol-Related Pancreatic Disease.Alcohol research : current reviews · 2017Review
- Release of Cathepsin B in Cytosol Causes Cell Death in Acute Pancreatitis.Gastroenterology · 2016Article
- Uptake of ascorbic acid by pancreatic acinar cells is negatively impacted by chronic alcohol exposure.American journal of physiology. Cell physiology · 2016Article
- Inhibition of pancreatic acinar mitochondrial thiamin pyrophosphate uptake by the cigarette smoke component 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Chronic Nicotine Exposure In Vivo and In Vitro Inhibits Vitamin B1 (Thiamin) Uptake by Pancreatic Acinar Cells.PloS one · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Thiamin is essential for normal metabolic activity of all mammalian cells, including those of the pancreas. Cells obtain thiamin from their surroundings and enzymatically convert it into thiamin pyrophosphate (TPP) in the cytoplasm; TPP is then taken up by mitochondria via a specific carrier the mitochondrial TPP transporter (MTPPT; product of the SLC25A19 gene). Chronic alcohol exposure negatively impacts the health of pancreatic acinar cells (PAC), but its effect on physiological/molecular parameters of MTPPT is not known. We addressed this issue using mouse pancreatic acinar tumor cell line 266-6 and primary PAC of wild-type and transgenic mice carrying the SLC25A19 promoter that were fed alcohol chronically. Chronic alcohol exposure of 266-6 cells (but not to its nonoxidative metabolites ethyl palmitate and ethyl oleate) led to a significant inhibition in mitochondrial TPP uptake, which was associated with a decreased expression of MTPPT protein, mRNA, and activity of the SLC25A19 promoter. Similarly, chronic alcohol feeding of mice led to a significant inhibition in expression of MTPPT protein, mRNA, heterogeneous nuclear RNA, as well as in activity of SLC25A19 promoter in PAC. While chronic alcohol exposure did not affect DNA methylation of the Slc25a19 promoter, a significant decrease in histone H3 euchromatin markers and an increase in H3 heterochromatin marker were observed. These findings show, for the first time, that chronic alcohol exposure negatively impacts pancreatic MTPPT, and that this effect is exerted, at least in part, at the level of Slc25a19 transcription and appears to involve epigenetic mechanism(s).
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