Opisthorchis viverrini excretory-secretory products suppress GLUT8 of cholangiocytes

Opisthorchis viverrini excretory-secretory products suppress GLUT8 of cholangiocytes

Opisthorchis viverrini infection and the subsequent bile duct cancer it induces remains a significant public health problem in Southeast Asia. Opisthorchiasis has been reported to cause reduced plasma glucose levels among infected patients. The underlying mechanism for this phenomenon is unclear. In...

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Published in:Parasitology research (1987) Vol. 123; no. 3; p. 161
Main Authors: Kha, Sandy, Chaiyadet, Sujittra, Saichua, Prasert, Tangkawatana, Sirikachorn, Sripa, Banchob, Suttiprapa, Sutas
Format: Journal Article
Language:English
Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-03-2024
Springer Nature B.V
Subjects:
Animals
Bile Duct Neoplasms
Bile ducts
Bile Ducts, Intrahepatic
Biomedical and Life Sciences
Biomedicine
Glucose
Glucose - metabolism
Humans
Immunoblotting
Immunology
Medical Microbiology
Microbiology
mRNA
Opisthorchiasis
Opisthorchis - metabolism
Opisthorchis viverrini
Public health
GLUT8
Diabetes
Expression
Cholangiocytes
Opisthorchis viverrini
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Summary:Opisthorchis viverrini infection and the subsequent bile duct cancer it induces remains a significant public health problem in Southeast Asia. Opisthorchiasis has been reported to cause reduced plasma glucose levels among infected patients. The underlying mechanism for this phenomenon is unclear. In the present study, evidence is presented to support the hypothesis that O. viverrini exploits host cholangiocyte glucose transporters (GLUTs) in a similar manner to that of rodent intestinal nematodes, to feed on unabsorbed glucose in the bile for survival. GLUT levels in a cholangiocyte H69 cell line co-cultured with excretory-secretory products of O. viverrini were examined using qPCR and immunoblotting. GLUT 8 mRNA and expressed proteins were found to be downregulated in H69 cells in the presence of O. viverrini . This suggests that O. viverrini alters glucose metabolism in cells within its vicinity by limiting transporter expression resulting in increased bile glucose that it can utilize and potentially explains the previously reported anti-insulin effect of opisthorchiasis.
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ISSN:0932-0113
1432-1955
DOI:10.1007/s00436-024-08184-3