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A Cellular Basis for Heightened Gut Sensitivity in Females.

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    This study reveals a new estrogen-driven pathway in the gut that increases sensitivity in females. This pathway involves communication between L-cells and enterochromaffin cells, potentially explaining sex differences in visceral pain disorders.

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    Area of Science:

    • Gastroenterology
    • Neuroscience
    • Endocrinology

    Background:

    • Visceral pain disorders like irritable bowel syndrome show a notable prevalence in females.
    • Enhanced communication between gut enterochromaffin (EC) cells and sensory nerves may underlie this sex bias.

    Purpose of the Study:

    • To identify a novel estrogen-responsive pathway contributing to increased gut sensitivity in females.
    • To elucidate the cellular and molecular mechanisms of this pathway.

    Main Methods:

    • Investigated estrogen receptor alpha (ERα) signaling in colonic L-cells and EC cells.
    • Analyzed the role of the SCFA receptor Olfr78 and peptide YY (PYY) in mediating cell-cell communication.
    • Examined the impact of PYY on EC cell serotonin release and gut pain.

    Main Results:

    • Estrogen signaling via ERα upregulates Olfr78 on L-cells, increasing PYY release and acetate sensitivity.
    • Elevated PYY activates NPY1R on neighboring EC cells, enhancing serotonin release.
    • This paracrine pathway increases gut sensitivity, particularly in females.

    Conclusions:

    • A novel estrogen-responsive paracrine pathway involving L-cells and EC cells increases gut sensitivity in females.
    • Hormonal fluctuations, stress, and diet can amplify this pathway, leading to maladaptive gut sensitivity.
    • This finding offers insights into the sex differences observed in visceral pain disorders.