In mice with inflammatory bowel disease or IPMK deficiency, consuming phytic acid at a dose of 2% of body weight increases HDAC3 activity, lowers acetylation at specific gene regions, reduces levels...
Mechanism
Synthesis from 1 study
A compound found in plants, called InsP6, turns on a molecular switch in gut cells that stops the production of enzymes that break down the seal between cells. When these enzymes aren't made, the seal stays strong, preventing the gut from leaking. This is how InsP6 fixes a damaged intestinal...
Most probable mechanism
A natural compound called InsP6 binds to a protein called HDAC3 in gut cells, turning it on. This activated HDAC3 removes a chemical tag from DNA that normally tells cells to make destructive enzymes. With the tag removed, those enzymes aren't made, so the glue holding gut cells together stays intact, preventing leaks in the intestinal lining.
InsP6 binds directly to HDAC3 associated with chromatin at gene promoters
InsP6 binding recruits the DAD domain of the NCoR1/2 corepressor complex to HDAC3, activating its deacetylase function
Activated HDAC3 removes acetyl groups from histone H4 at lysine 16 specifically at promoters of matrix metalloproteinase genes
Deacetylation of H4K16 represses transcription of matrix metalloproteinase genes, reducing their protein expression
Reduced matrix metalloproteinase levels prevent degradation of tight junction proteins such as ZO-1 and occludin
Preserved tight junction integrity reduces paracellular permeability and restores intestinal barrier function
Evidence from Studies
Supporting (1)
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Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function
Contradicting (0)
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