The DOI matches its Crossref record; 49 of the 50 references it cites were found in a registry or an index.
The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction
Open accessAbstract
Disruption of the intestinal barrier is a causal factor in the development of alcoholic endotoxemia and hepatitis. This study was undertaken to determine whether zinc deficiency is related to the deleterious effects of alcohol on the intestinal barrier. Mice were pair fed an alcohol or isocaloric liquid diet for 4 wk, and hepatitis was detected in association with elevated blood endotoxin level. Alcohol exposure significantly increased the permeability of the ileum but did not affect the barrier function of the duodenum or jejunum. Reduction of tight-junction proteins at the ileal epithelium was detected in alcohol-fed mice although alcohol exposure did not cause apparent histopathological changes. Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species. Caco-2 cell culture demonstrated that alcohol exposure increases the intracellular free zinc because of oxidative stress. Zinc deprivation caused epithelial barrier disruption in association with disassembling of tight junction proteins in the Caco-2 monolayer cells. Furthermore, minor zinc deprivation exaggerated the deleterious effect of alcohol on the epithelial barrier. In conclusion, epithelial barrier dysfunction in the distal small intestine plays an important role in alcohol-induced gut leakiness, and zinc deficiency attributable to oxidative stress may interfere with the intestinal barrier function by a direct action on tight junction proteins or by sensitizing to the effects of alcohol.
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“binge alcohol exposure [232], [233], [234], [235], [236], [237], [238], [239] and nonalcoholic substances including fructose [240], [241], [242] are known to promote gut leakiness, contributing to more severe inflammatory liver disease.”
In the citing paper
“binge alcohol exposure [232], [233], [234], [235], [236], [237], [238], [239] and nonalcoholic substances including fructose [240], [241], [242] are known to promote gut leakiness, contributing to more severe inflammatory liver disease.”
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Cites
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Tight junctions and the modulation of barrier function in disease
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Intestinal barrier: An interface between health and disease
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THE LEAKY GUT OF ALCOHOLISM: POSSIBLE ROUTE OF ENTRY FOR TOXIC COMPOUNDS
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Loss of the Tight Junction Protein ZO-1 in Dextran Sulfate Sodium Induced Colitis
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Zinc Oxide Protects Cultured Enterocytes from the Damage Induced by Escherichia coli
Roselli, M., Finamore, A., Garaguso, I., Britti, M. S., & Mengheri, E. (2003) · Journal of Nutrition · doi:10.1093/jn/133.12.4077 · Cited by 391
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Cited by
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Gut–Liver Axis in Alcoholic Liver Disease
Szabo, G. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.10.042 · Cited by 754
The Role of Zinc in Antiviral Immunity
Read, S. A., Obeid, S., Ahlenstiel, C., & Ahlenstiel, G. (2019) · Advances in Nutrition · doi:10.1093/advances/nmz013 · Cited by 801
Wang, Y., Kirpich, I., Liu, Y., Ma, Z., Barve, S. S., McClain, C. J., & Feng, W. (2011) · American Journal Of Pathology · doi:10.1016/j.ajpath.2011.08.039 · Cited by 255
Self-citationMohammad, M. K., Zhou, Z., Cave, M. C., Barve, A. J., & McClain, C. J. (2012) · Nutrition in Clinical Practice · doi:10.1177/0884533611433534 · Cited by 248
Self-citationPotential mechanisms for the emerging link between obesity and increased intestinal permeability
Teixeira, T. F. S., Collado, M. C., Ferreira, C. L. D. L. F., Bressan, J., & Pelúzio, M. D. C. G. (2012) · Nutrition Research · doi:10.1016/j.nutres.2012.07.003 · Cited by 255
Metadata
- Authors
- Zhong, W., McClain, C. J., Cave, M., Kang, Y. J., & Zhou, Z.
- Affiliations
- China Agricultural University (CN)
- University of Louisville (US)
- Corresponding author
- Zhou, Zhanxiang
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2010-05
- Volume
- 298
- Issue
- 5
- Pages
- G625-G633
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- PMC
- PMC2867425
- OpenAlex
- W2140449647
- Cited by
- 214
- References
- 50
- Citations by year
- 2026: 5 · 2025: 14 · 2024: 13 · 2023: 17 · 2022: 12 · 2021: 12 · 2020: 15 · 2019: 12 · 2018: 7 · 2017: 13 · 2016: 7 · 2015: 24 · 2014: 19 · 2013: 16 · 2012: 16
- FWCI
- 9.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (R01AA018016, K23AA018399, R01AA018869, R01AA014623)
- National Institute of Environmental Health Sciences (R01ES021375)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- zinc deficiency, alcohol, intestinal barrier dysfunction, tight junction proteins, intestinal permeability, ileum, oxidative stress, reactive oxygen species, endotoxemia, alcoholic hepatitis, leaky gut, Caco-2 cells
- MeSH terms
- Alcohol Drinking, Ethanol, Animals, Humans, Ileum, Intestines, Liver Diseases, Alcoholic, Male, Mice, Inbred C57BL, Permeability, Zinc, Reactive Oxygen Species, Oxidative Stress, Caco-2 Cells, Tight Junctions, Mice
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