Confirmation that OCTN2 is downregulated in IBDs - alt.support.food-allergies

Message from discussion Confirmation that OCTN2 is downregulated in IBDs
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From: Kofi <k...@anon.un>
Newsgroups: sci.life-extension,alt.support.food-allergies,alt.support.ibs,alt.support.celiac,alt.support.crohns-colitis
Subject: Re: Confirmation that OCTN2 is downregulated in IBDs
Organization: UN
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In article 
<edd2ecbf-aa30-45c8-84fe-d0af18522...@p20g2000vbl.googlegroups.com>, 
jay <jaym1...@hotmail.com> wrote:

> > 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
> causes IBD or that OCTN2 is simply reduced during inflammation?

Given that supplemental carnitine in liposomes has alleviated TNBS 
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