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The author of the following post on LE, Kofi, is a genious in my eyes. Nobody knows more about intestinal permeability (leaky gut) or BBB disruption.
Does anyone know how to increase Butyrate? I read that fiber or resistant starch is a good way to go.
http://groups.google.com/group/sci....8333a?lnk=gst&q=kofi+barrier#28aa1babe368333a
This suggests that a number of AMPK activators - like calorie
restriction - could be useful for leaky gut conditions and it links
intestinal barrier function to an important longevity pathway. It puts
butyrate production in the gut from dietary fiber right in the middle of
a number of problems, including longevity research, cancer prevention,
insulin sensitivity, innate immunity and autoimmunity.
J Nutr. 2009 Sep;139(9):1619-25. Epub 2009 Jul 22.
Butyrate enhances the intestinal barrier by facilitating tight junction
assembly via activation of AMP-activated protein kinase in Caco-2 cell
monolayers.
Peng L, Li ZR, Green RS, Holzman IR, Lin J.
Department of Pediatrics, Mount Sinai School of Medicine, New York, NY
10029-6574, USA.
Butyrate, one of the SCFA, promotes the development of the intestinal
barrier. However, the molecular mechanisms underlying the butyrate
regulation of the intestinal barrier are unknown. To test the hypothesis
that the effect of butyrate on the intestinal barrier is mediated by the
regulation of the assembly of tight junctions involving the activation
of the AMP-activated protein kinase (AMPK), we determined the effect of
butyrate on the intestinal barrier by measuring the transepithelial
electrical resistance (TER) and inulin permeability in a Caco-2 cell
monolayer model. We further used a calcium switch assay to study the
assembly of epithelial tight junctions and determined the effect of
butyrate on the assembly of epithelial tight junctions and AMPK
activity. We demonstrated that the butyrate treatment increased AMPK
activity and accelerated the assembly of tight junctions as shown by the
reorganization of tight junction proteins, as well as the development of
TER. AMPK activity was also upregulated by butyrate during calcium
switch-induced tight junction assembly. Compound C, a specific AMPK
inhibitor, inhibited the butyrate-induced activation of AMPK. The
facilitating effect of butyrate on the increases in TER in standard
culture media, as well as after calcium switch, was abolished by
compound C. We conclude that butyrate enhances the intestinal barrier by
regulating the assembly of tight junctions. This dynamic process is
mediated by the activation of AMPK. These results suggest an intriguing
link between SCFA and the intracellular energy sensor for the
development of the intestinal barrier.
PMID: 19625695
Does anyone know how to increase Butyrate? I read that fiber or resistant starch is a good way to go.
http://groups.google.com/group/sci....8333a?lnk=gst&q=kofi+barrier#28aa1babe368333a
This suggests that a number of AMPK activators - like calorie
restriction - could be useful for leaky gut conditions and it links
intestinal barrier function to an important longevity pathway. It puts
butyrate production in the gut from dietary fiber right in the middle of
a number of problems, including longevity research, cancer prevention,
insulin sensitivity, innate immunity and autoimmunity.
J Nutr. 2009 Sep;139(9):1619-25. Epub 2009 Jul 22.
Butyrate enhances the intestinal barrier by facilitating tight junction
assembly via activation of AMP-activated protein kinase in Caco-2 cell
monolayers.
Peng L, Li ZR, Green RS, Holzman IR, Lin J.
Department of Pediatrics, Mount Sinai School of Medicine, New York, NY
10029-6574, USA.
Butyrate, one of the SCFA, promotes the development of the intestinal
barrier. However, the molecular mechanisms underlying the butyrate
regulation of the intestinal barrier are unknown. To test the hypothesis
that the effect of butyrate on the intestinal barrier is mediated by the
regulation of the assembly of tight junctions involving the activation
of the AMP-activated protein kinase (AMPK), we determined the effect of
butyrate on the intestinal barrier by measuring the transepithelial
electrical resistance (TER) and inulin permeability in a Caco-2 cell
monolayer model. We further used a calcium switch assay to study the
assembly of epithelial tight junctions and determined the effect of
butyrate on the assembly of epithelial tight junctions and AMPK
activity. We demonstrated that the butyrate treatment increased AMPK
activity and accelerated the assembly of tight junctions as shown by the
reorganization of tight junction proteins, as well as the development of
TER. AMPK activity was also upregulated by butyrate during calcium
switch-induced tight junction assembly. Compound C, a specific AMPK
inhibitor, inhibited the butyrate-induced activation of AMPK. The
facilitating effect of butyrate on the increases in TER in standard
culture media, as well as after calcium switch, was abolished by
compound C. We conclude that butyrate enhances the intestinal barrier by
regulating the assembly of tight junctions. This dynamic process is
mediated by the activation of AMPK. These results suggest an intriguing
link between SCFA and the intracellular energy sensor for the
development of the intestinal barrier.
PMID: 19625695