kiny
Well-known member
- Joined
- Apr 28, 2011
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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/
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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].
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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].
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