Molecular analysis of the effect of short-chain fatty acids on intestinal cell proliferation

Short-chain fatty acids (SCFA), particularly butyrate, were shown to regulate cell proliferation in vitro and in vivo. Indeed, butyrate is the major fuel for colonic epithelial cells, and it can influence cell proliferation through the release of growth factors or gastrointestinal peptides such as g...

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Bibliographic Details
Published in:Proceedings of the Nutrition Society 2003-02, Vol.62 (1), p.101-106
Main Authors: Blottiere, Herve M., Buecher, Bruno, Galmiche, Jean-Paul, Cherbut, Christine
Format: Article
Language:English
Subjects:
Acetylation - drug effects
blood flow
butyrates
Butyrates - pharmacology
cell cycle
Cell Cycle - drug effects
Cell Division - drug effects
cell proliferation
Colon - cytology
Colon - drug effects
Cyclin D3
cyclin-dependent kinase
Cyclin-Dependent Kinase Inhibitor p21
Cyclins - genetics
Cyclins - metabolism
epithelial cells
Epithelial Cells - drug effects
Epithelial Cells - metabolism
Fatty acids
Fatty Acids, Volatile - pharmacology
Food and Nutrition
gastrins
gastrointestinal system
Gene Expression
genes
Growth factors
histone deacetylase
Histone Deacetylase Inhibitors
histones
Humans
Intestinal Mucosa - cytology
Intestinal Mucosa - drug effects
Life Sciences
Peptides
Session: Short-chain fatty acids
short chain fatty acids
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Summary:Short-chain fatty acids (SCFA), particularly butyrate, were shown to regulate cell proliferation in vitro and in vivo. Indeed, butyrate is the major fuel for colonic epithelial cells, and it can influence cell proliferation through the release of growth factors or gastrointestinal peptides such as gastrin, or through modulation of mucosal blood flow. Lastly, SCFA can act directly on genes regulating cell proliferation, and butyrate is the main SCFA to display such an effect. Butyrate inhibits histone deacetylase, which will allow histone hyperacetylation. Such hyperacetylation leads to transcription of several genes, including p21/Cipl. Moreover, it will allow cyclin D3 hyper-expression by inhibiting its degradation. The induction of the cyclin-dependent kinase inhibitory protein p21/Cipl accounts for cell arrest in the Gl phase of the cell cycle. However, in the absence of p21 other mechanisms are initiated, leading to inhibition of cell proliferation.
ISSN:0029-6651
1475-2719
DOI:10.1079/PNS2002215