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06-24-2012, 02:34 AM   #1
kiny
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Butyrate

Hm, so I have seen some crohn diets (SCD being one of them) that are critiqued by biologists for crohn's disease because they are lacking SCFA (short chain fatty acids). The problem isn't the lack of of carbs, it's the lack of SCFA that is the result of trying to avoid every food group that has carbs. So the one of importance to us is called butyrate.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295784/

"
We demonstrate that, in all CrD colonic tissues, butyrate reduced p65 phosphorylation and release of pro-inflammatory cytokines, such as TNF-α and COX-2 or ICAM-1 from mucosal mononuclear cells, thus restoring the pattern observed in controls after challenge with LPS from Escherichia Coli. Our study suggests that the restoration of intracellular ROS balance through appropriate control of the redox machinery may be a novel approach to treatment of CrD and may pave the way for the development of a new class of functional foods that, by enhancing butyrate production, could be effective treatments for CrD.

ELISA

TNF-α secretion was measured using the BD OptEIATM ELISA kit II (BD Biosciences) according to the manufacturer's instructions. Protein concentrations of whole-cell lysates were measured using the BioRad Dc protein Assay (BioRad). TNF-α levels were normalized to standard protein concentrations [30].


Discussion

This report describes the relationships among a bacterial product, oxidative stress and mucosal inflammation in the mucosa of patients with CrD. We have identified butyrate's role in intestinal epithelial homeostasis by promoting anti-oxidative responses and inhibiting mucosal inflammation in the colon of CrD patients.

The short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of dietary fibers, plays a major role in the physiology of the colonic mucosa. It is also the major oxidative substrate for the colonocyte [34]. Impairment of IEC energy homeostasis is a typical feature of inflamed tissue in CrD. Constitutive energy expenditure mediated by persistent IEC activation and reduced energy supply may be the main causes of failure of IEC to preserve energy homeostasis [35].

Several studies report decreased butyrate oxidation in the inflamed mucosa of patients suffering from UC [36] or CrD [37] and in animal models of experimental colitis [38]. Although other studies found no defect in butyrate oxidation during IBD [39],[40],[41].

"
06-24-2012, 02:55 AM   #2
kiny
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http://onlinelibrary.wiley.com/doi/1...05.02639.x/pdf

"SUMMARY

Background: Butyrate exerts anti-inflammatory effects in
experimental colitis and on Crohn’s disease lamina
propria mononuclear cells in vitro.

Aim: To explore the efficacy and safety of oral butyrate
in Crohn’s disease.

Methods: Thirteen patients with mild–moderate ileocolonic
Crohn’s disease received 4 g/day butyrate as
enteric-coated tablets for 8 weeks. Full colonoscopy
and ileoscopy were performed before and after treatment.
Endoscopical and histological score, laboratory
data, Crohn’s disease activity index and mucosal
interleukin (IL)-1b, IL-6, IL-12, interferon-c, tumour
necrosis factor-a and nuclear factor-kappa B (NF-jB)
were assessed before and after treatment.

Results: One patient withdrew from the study, and
three patients did not experience clinical improvement.
Among the nine patients (69%) who responded to
treatment, seven (53%) achieved remission and two
had a partial response. Endoscopical and histological
score significantly improved after treatment at ileocaecal
level (P < 0.05). Leucocyte blood count, erythrocyte
sedimentation rate and mucosal levels of NF-jB
and IL-1b significantly decreased after treatment
(P < 0.05).

Conclusions: Oral butyrate is safe and well tolerated, and
may be effective in inducing clinical improvement/
remission in Crohn’s disease. These data indicate the
need for a large investigation to extend the present
findings, and suggest that butyrate may exert its action
through downregulation of NF-jB and IL-1b."
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