Metabolism of sphingolipids in the gut and its relation to inflammation and cancer development.
(2009) In Progress in lipid research 48(1). p.62-72- Abstract
- Sphingolipids are abundant in the microvillar membrane of intestinal epithelial cells where they are essential for structural integrity and may act as receptors for toxins, virus and bacteria. Metabolism of dietary and membrane sphingolipids in the intestine generates ceramide, sphingosine, sphingosine-1-phosphate, and ceramide-1-phosphate, via the action of alkaline sphingomyelinase, neutral ceramidase, sphingosine-1-kinase, and ceramide-1-kinase. These intermediary metabolites act as bioactive lipid messengers, influencing numerous cellular functions including growth, differentiation and apoptosis of both epithelial and immunocompetent cells in the gastrointestinal tract, and also the progress of inflammation and responsiveness of the... (More)
- Sphingolipids are abundant in the microvillar membrane of intestinal epithelial cells where they are essential for structural integrity and may act as receptors for toxins, virus and bacteria. Metabolism of dietary and membrane sphingolipids in the intestine generates ceramide, sphingosine, sphingosine-1-phosphate, and ceramide-1-phosphate, via the action of alkaline sphingomyelinase, neutral ceramidase, sphingosine-1-kinase, and ceramide-1-kinase. These intermediary metabolites act as bioactive lipid messengers, influencing numerous cellular functions including growth, differentiation and apoptosis of both epithelial and immunocompetent cells in the gastrointestinal tract, and also the progress of inflammation and responsiveness of the mucosal cells to pathogens. This review summarizes background and recent progress in the metabolism of dietary and endogenous sphingolipids in the gut and its pathophysiological implications. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1271176
- author
- Duan, Rui-Dong LU and Nilsson, Åke LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Progress in lipid research
- volume
- 48
- issue
- 1
- pages
- 62 - 72
- publisher
- Elsevier
- external identifiers
-
- wos:000262563300005
- pmid:19027789
- scopus:57649188727
- pmid:19027789
- ISSN
- 1873-2194
- DOI
- 10.1016/j.plipres.2008.04.003
- language
- English
- LU publication?
- yes
- id
- 052de26c-ff4b-467a-a002-a82a99047e46 (old id 1271176)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19027789?dopt=Abstract
- date added to LUP
- 2016-04-04 09:09:52
- date last changed
- 2024-01-12 09:38:33
@article{052de26c-ff4b-467a-a002-a82a99047e46, abstract = {{Sphingolipids are abundant in the microvillar membrane of intestinal epithelial cells where they are essential for structural integrity and may act as receptors for toxins, virus and bacteria. Metabolism of dietary and membrane sphingolipids in the intestine generates ceramide, sphingosine, sphingosine-1-phosphate, and ceramide-1-phosphate, via the action of alkaline sphingomyelinase, neutral ceramidase, sphingosine-1-kinase, and ceramide-1-kinase. These intermediary metabolites act as bioactive lipid messengers, influencing numerous cellular functions including growth, differentiation and apoptosis of both epithelial and immunocompetent cells in the gastrointestinal tract, and also the progress of inflammation and responsiveness of the mucosal cells to pathogens. This review summarizes background and recent progress in the metabolism of dietary and endogenous sphingolipids in the gut and its pathophysiological implications.}}, author = {{Duan, Rui-Dong and Nilsson, Åke}}, issn = {{1873-2194}}, language = {{eng}}, number = {{1}}, pages = {{62--72}}, publisher = {{Elsevier}}, series = {{Progress in lipid research}}, title = {{Metabolism of sphingolipids in the gut and its relation to inflammation and cancer development.}}, url = {{https://lup.lub.lu.se/search/files/5249217/1360626.pdf}}, doi = {{10.1016/j.plipres.2008.04.003}}, volume = {{48}}, year = {{2009}}, }