Experimental Colitis: Decreased Octn2 and Atb0+ Expression in Rat Colonocytes Induces Carnitine Depletion That is Reversible by Carnitine-loaded Liposomes.
From: Gastroenterology Unit, Department of Clinical and Experimental Medicine, University Federico II, Naples, Italy.
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology
- Publish Date: Dec 2006
- ISSN: 1530-6860
- Volume: 20
- Issue: 14
- Pages: 2544-6
- Medium: Internet
- Language: English
- Citation (JAMA): D'Argenio Giuseppe, Calvani Menotti, Casamassimi Amelia, et al. Experimental Colitis: Decreased Octn2 and Atb0+ Expression in Rat Colonocytes Induces Carnitine Depletion That is Reversible by Carnitine-loaded Liposomes.. FASEB J. Dec 2006;20:2544-6
Abstract
Carnitine transporters have recently been implicated in susceptibility to inflammatory bowel disease (IBD). Because carnitine is required for beta-oxidation, it was suggested that decreased carnitine transporters, and hence reduced carnitine uptake, could lead to impaired fatty acid oxidation in intestinal epithelial cells, and to cell injury. We investigated this issue by examining the expression of the carnitine transporters OCTN2 and ATB0+, and butyrate metabolism in colonocytes in a rat model of IBD induced by trinitrobenzene sulfonic acid (TNBS). We found that Octn2 and Atb0+ expression was decreased in inflammatory samples at translational and functional level. Butyrate oxidation, evaluated based on CO2 production and acetyl-coenzyme A synthesis, was deranged in colonocytes from TNBS-treated rats. Treatment with carnitine-loaded liposomes corrected the butyrate metabolic alterations in vitro and reduced the severity of colitis in vivo. These results suggest that carnitine depletion in colonocytes is associated with the inability of mitochondria to maintain normal butyrate beta-oxidation. Our data indicate that carnitine is a rate-limiting factor for the maintenance of physiological butyrate oxidation in colonic cells. This hypothesis could also explain the contradictory therapeutic efficacy of butyrate supplementation observed in clinical trials of IBD.
Mesh Headings (Keywords): Amino Acid Sequence, Amino Acid Transport System ASC, Animals, Base Sequence, Butyric Acid, Carnitine, Colitis, Liposomes, Molecular Sequence Data, Neurotransmitter Transport Proteins, Organic Cation Transport Proteins, Rats, Rats, Wistar, Trinitrobenzenesulfonic Acid
Check for Full Text / PubMed Unique Identifier (PMID): 17065219
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.