The bacterium Lactobacillus vaginalis can break down zinc bound to phytate in wheat bran, releasing zinc and specific inositol phosphate compounds that may be more easily absorbed by the body.
Mechanism
Synthesis from 1 study
Good bacteria in the gut break down a plant-based zinc compound into pieces that help seal the gut lining and turn off inflammation signals. This dual action protects the intestine and improves zinc absorption.
Most probable mechanism
Good bacteria in the gut break down a zinc-containing compound from plant material into smaller pieces that the body can use. These pieces help seal the gut lining and calm down inflammation by turning off signals that cause swelling.
Zinc phytate, whether enzymatically hydrolyzed or in its standard form, is metabolized by Lactobacillus vaginalis into inositol phosphates (IP3, IP4, IP5) and ionic zinc.
Ionic zinc and inositol phosphates activate HDAC3 in intestinal epithelial cells, leading to increased production of tight junction proteins ZO-1 and occludin.
Increased ZO-1 and occludin enhance the structural integrity of the intestinal barrier, reducing permeability and preventing leakage of harmful substances.
Ionic zinc and inositol phosphates inhibit the PI3K/AKT signaling pathway, preventing activation of NF-κB and reducing transcription of pro-inflammatory cytokines.
Reduced NF-κB activity lowers levels of inflammatory mediators such as TNF-α and IL-6, attenuating intestinal inflammation.
Less supported by current evidence, but not ruled out
The presence of certain good bacteria changes the types of bile acids in the gut, which then bind to receptors in the gut lining to help seal it and reduce swelling.
Lactobacillus vaginalis proliferation alters gut microbiota composition, favoring bacterial conversion of primary bile acids into secondary bile acids.
Secondary bile acids, including chenodeoxycholic acid and lithocholic acid, bind to nuclear receptors FXR and VDR in intestinal epithelial cells.
Activation of FXR and VDR promotes expression of tight junction proteins and suppresses inflammatory signaling pathways.
Evidence from Studies
Supporting (1)
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Contradicting (0)
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