When the biochemical interaction between phytic acid and HDAC3 is interrupted, it results in a weakening of the intestinal barrier and a rise in inflammatory markers throughout the body.
Mechanism
Synthesis from 2 studies
Phytic acid turns on a molecular switch that stops gut-damaging enzymes from being made. Without it, those enzymes break apart the seal between gut cells, letting harmful substances leak into the body and cause inflammation. Adding phytic acid fixes the seal and stops the leak.
Most probable mechanism
When phytic acid is present, it binds to a protein called HDAC3 in the gut lining, which turns off genes that make enzymes that break down the glue holding gut cells together. Without this control, those enzymes tear apart the barrier, letting substances leak into the bloodstream and trigger inflammation. Adding phytic acid restores the control and seals the gut.
Phytic acid binds directly to HDAC3 on chromatin and recruits the DAD domain of the NCoR1/2 corepressor complex, activating HDAC3's enzymatic function.
Activated HDAC3 removes acetyl groups from histone H4 at lysine 16 at the promoters of matrix metalloproteinase (MMP) genes.
Deacetylation of histone H4K16 represses transcription of MMP genes, including MMP1, MMP3, MMP10, and MMP13.
Reduced MMP expression decreases secretion of proteolytic enzymes that degrade tight junction proteins such as ZO-1 and occludin.
Preservation of tight junction proteins maintains low paracellular permeability in the intestinal epithelium.
Intact intestinal barrier prevents translocation of luminal contents into systemic circulation, suppressing activation of immune responses and systemic inflammation.
Evidence from Studies
Supporting (2)
Community contributions welcome
Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function
Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function
Contradicting (0)
Community contributions welcome
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