A modified form of zinc from wheat bran increases the production of proteins that strengthen the gut lining and reduces activity in a signaling pathway linked to inflammation in mice with induced...
Mechanism
Synthesis from 1 study
The compound is broken down by gut bacteria into zinc and related molecules that enter gut cells. These molecules strengthen the seal between gut cells by turning on a key regulator called HDAC3, while also shutting down a major inflammation pathway. Together, this keeps the gut lining intact and...
Most probable mechanism
A compound from wheat bran is broken down by gut bacteria into zinc and special molecules that enter intestinal cells. These molecules turn on a protein called HDAC3, which helps seal the gaps between cells in the gut lining. At the same time, they block a chain of signals that would otherwise cause inflammation, keeping the gut lining intact and preventing leaks.
Enzymatically hydrolyzed wheat bran-derived zinc phytate is metabolized by gut microbiota into bioavailable inositol phosphates and ionic zinc
Ionic zinc and inositol phosphates activate HDAC3 expression in colonic epithelial cells
HDAC3 activation increases transcription of tight junction proteins ZO-1 and occludin, enhancing structural integrity of the intestinal barrier
Ionic zinc and inositol phosphates inhibit phosphorylation of PI3K and AKT, preventing downstream activation of NF-κB
Suppressed NF-κB nuclear translocation reduces transcription of pro-inflammatory cytokines, attenuating mucosal inflammation
Combined upregulation of tight junction proteins and suppression of inflammatory signaling restores intestinal barrier function and reduces permeability
Less supported by current evidence, but not ruled out
Changes in gut bacteria caused by the compound lead to increased production of certain bile acids, which bind to receptors in intestinal cells and may help tighten the barrier and reduce inflammation.
Gut microbiota composition shifts in response to the compound, increasing populations of bacteria capable of converting primary bile acids to secondary forms
Secondary bile acids chenodeoxycholic acid and lithocholic acid accumulate in the colon
Elevated secondary bile acids bind to nuclear receptors FXR and VDR in intestinal epithelial cells
Activated FXR and VDR promote expression of barrier proteins and suppress inflammatory pathways
Evidence from Studies
Supporting (1)
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Contradicting (0)
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