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Newsgroups: sci.life-extension, alt.support.food-allergies, alt.support.ibs, alt.support.celiac, alt.support.crohns-colitis
From: Kofi <k...@anon.un>
Date: Sun, 21 Jun 2009 16:30:28 -0600
Local: Mon, Jun 22 2009 8:30 am
Subject: Re: Confirmation that OCTN2 is downregulated in IBDs
In article
<edd2ecbf-aa30-45c8-84fe-d0af18522...@p20g2000vbl.googlegroups.com>, jay <jaym1...@hotmail.com> wrote: Given that supplemental carnitine in liposomes has alleviated TNBS > > OCTN2 is upregulated by intermittent fasting, exercise, PPARalpha > > agonists and, I think, testosterone. It's vital for carnitine uptake > > (which is antiinflammatory in the gut) and butyrate metabolism (crucial > > for HDAC inhibition). > > > > Changes in mRNA expression levels of solute carrier transporters in > > inflammatory bowel disease patients... > Does the study distinguish if OCTN2 (carnitine transporter) reduction colitis in mice when TNBS downregulates OCTN2, I'd say it's causative [PMID 17065219]. The other limiting factor might be glutamine (via the Atb0+ transporter). > Since
> carnitine is an antioxidant and is essential for metabolism of long > chain fatty acids (LCFAs), lack of it could cause inflammation. On the > other hand, during inflammation, cell many not want to metabolize > LCFAs since they are prone to peroxidation You must Sign in before you can post messages.
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