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Bile Acids in Pancreatic Carcinogenesis

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Title: Bile Acids in Pancreatic Carcinogenesis
Authors: Bharti Sharma, Kate Twelker, Cecilia Nguyen, Scott Ellis, Navin D. Bhatia, Zachary Kuschner, Andrew Agriantonis, George Agriantonis, Monique Arnold, Jasmine Dave, Juan Mestre, Zahra Shafaee, Shalini Arora, Hima Ghanta, Jennifer Whittington
Source: Metabolites, Vol 14, Iss 7, p 348 (2024)
Publisher Information: MDPI AG, 2024.
Publication Year: 2024
Collection: LCC:Microbiology
Subject Terms: pancreatic cancer, bile acids, genetic alteration, tumorigenesis, Microbiology, QR1-502
More Details: Pancreatic cancer (PC) is a dangerous digestive tract tumor that is becoming increasingly common and fatal. The most common form of PC is pancreatic ductal adenocarcinoma (PDAC). Bile acids (BAs) are closely linked to the growth and progression of PC. They can change the intestinal flora, increasing intestinal permeability and allowing gut microbes to enter the bloodstream, leading to chronic inflammation. High dietary lipids can increase BA secretion into the duodenum and fecal BA levels. BAs can cause genetic mutations, mitochondrial dysfunction, abnormal activation of intracellular trypsin, cytoskeletal damage, activation of NF-κB, acute pancreatitis, cell injury, and cell necrosis. They can act on different types of pancreatic cells and receptors, altering Ca2+ and iron levels, and related signals. Elevated levels of Ca2+ and iron are associated with cell necrosis and ferroptosis. Bile reflux into the pancreatic ducts can speed up the kinetics of epithelial cells, promoting the development of pancreatic intraductal papillary carcinoma. BAs can cause the enormous secretion of Glucagon-like peptide-1 (GLP-1), leading to the proliferation of pancreatic β-cells. Using Glucagon-like peptide-1 receptor agonist (GLP-1RA) increases the risk of pancreatitis and PC. Therefore, our objective was to explore various studies and thoroughly examine the role of BAs in PC.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2218-1989
Relation: https://www.mdpi.com/2218-1989/14/7/348; https://doaj.org/toc/2218-1989
DOI: 10.3390/metabo14070348
Access URL: https://doaj.org/article/19f154169ca4404fbb02ffdcdebe2e27
Accession Number: edsdoj.19f154169ca4404fbb02ffdcdebe2e27
Database: Directory of Open Access Journals
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  Data: Bile Acids in Pancreatic Carcinogenesis
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  Data: <searchLink fieldCode="AR" term="%22Bharti+Sharma%22">Bharti Sharma</searchLink><br /><searchLink fieldCode="AR" term="%22Kate+Twelker%22">Kate Twelker</searchLink><br /><searchLink fieldCode="AR" term="%22Cecilia+Nguyen%22">Cecilia Nguyen</searchLink><br /><searchLink fieldCode="AR" term="%22Scott+Ellis%22">Scott Ellis</searchLink><br /><searchLink fieldCode="AR" term="%22Navin+D%2E+Bhatia%22">Navin D. Bhatia</searchLink><br /><searchLink fieldCode="AR" term="%22Zachary+Kuschner%22">Zachary Kuschner</searchLink><br /><searchLink fieldCode="AR" term="%22Andrew+Agriantonis%22">Andrew Agriantonis</searchLink><br /><searchLink fieldCode="AR" term="%22George+Agriantonis%22">George Agriantonis</searchLink><br /><searchLink fieldCode="AR" term="%22Monique+Arnold%22">Monique Arnold</searchLink><br /><searchLink fieldCode="AR" term="%22Jasmine+Dave%22">Jasmine Dave</searchLink><br /><searchLink fieldCode="AR" term="%22Juan+Mestre%22">Juan Mestre</searchLink><br /><searchLink fieldCode="AR" term="%22Zahra+Shafaee%22">Zahra Shafaee</searchLink><br /><searchLink fieldCode="AR" term="%22Shalini+Arora%22">Shalini Arora</searchLink><br /><searchLink fieldCode="AR" term="%22Hima+Ghanta%22">Hima Ghanta</searchLink><br /><searchLink fieldCode="AR" term="%22Jennifer+Whittington%22">Jennifer Whittington</searchLink>
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  Data: Metabolites, Vol 14, Iss 7, p 348 (2024)
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  Data: MDPI AG, 2024.
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  Data: LCC:Microbiology
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  Data: <searchLink fieldCode="DE" term="%22pancreatic+cancer%22">pancreatic cancer</searchLink><br /><searchLink fieldCode="DE" term="%22bile+acids%22">bile acids</searchLink><br /><searchLink fieldCode="DE" term="%22genetic+alteration%22">genetic alteration</searchLink><br /><searchLink fieldCode="DE" term="%22tumorigenesis%22">tumorigenesis</searchLink><br /><searchLink fieldCode="DE" term="%22Microbiology%22">Microbiology</searchLink><br /><searchLink fieldCode="DE" term="%22QR1-502%22">QR1-502</searchLink>
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  Label: Description
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  Data: Pancreatic cancer (PC) is a dangerous digestive tract tumor that is becoming increasingly common and fatal. The most common form of PC is pancreatic ductal adenocarcinoma (PDAC). Bile acids (BAs) are closely linked to the growth and progression of PC. They can change the intestinal flora, increasing intestinal permeability and allowing gut microbes to enter the bloodstream, leading to chronic inflammation. High dietary lipids can increase BA secretion into the duodenum and fecal BA levels. BAs can cause genetic mutations, mitochondrial dysfunction, abnormal activation of intracellular trypsin, cytoskeletal damage, activation of NF-κB, acute pancreatitis, cell injury, and cell necrosis. They can act on different types of pancreatic cells and receptors, altering Ca2+ and iron levels, and related signals. Elevated levels of Ca2+ and iron are associated with cell necrosis and ferroptosis. Bile reflux into the pancreatic ducts can speed up the kinetics of epithelial cells, promoting the development of pancreatic intraductal papillary carcinoma. BAs can cause the enormous secretion of Glucagon-like peptide-1 (GLP-1), leading to the proliferation of pancreatic β-cells. Using Glucagon-like peptide-1 receptor agonist (GLP-1RA) increases the risk of pancreatitis and PC. Therefore, our objective was to explore various studies and thoroughly examine the role of BAs in PC.
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  Data: 2218-1989
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  Data: 10.3390/metabo14070348
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      – SubjectFull: bile acids
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      – SubjectFull: genetic alteration
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