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Gut bitter taste receptor signalling induces ABCB1 through a mechanism involving CCK

Tae-Il Jeon1, Young-Kyo Seo, Timothy F Osborne

  • 1Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA.

The Biochemical Journal
|May 20, 2011
PubMed

Insights

Bitter taste receptors (T2Rs) in the gut signal through cholecystokinin (CCK) to activate ABCB1 transporters. This mechanism helps limit the absorption of dietary toxins, protecting the body.

Area of Science:

  • Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • Bitter taste-sensing type 2 receptors (T2Rs) are found in the oral cavity and gut.
  • Their role in gut enteroendocrine cells is not well understood.
  • Previous research suggested T2R-dependent cholecystokinin (CCK) secretion limits toxin absorption, but an active mechanism was missing.

Purpose of the Study:

  • To investigate the mechanism by which T2R signaling influences the absorption of dietary toxins in the intestine.
  • To determine if T2R activation leads to the regulation of efflux transporters like ABCB1 (ATP-binding cassette B1).

Main Methods:

  • Treated intestinal cells and mouse intestine with phenylthiocarbamide (PTC), a T2R38 agonist.
  • Utilized T2R38 siRNA and a gastrin receptor antagonist (YM022) to block signaling pathways.
  • Measured ABCB1 expression and efflux activity.

Main Results:

  • PTC stimulation of T2R38 increased ABCB1 expression in intestinal cells and mouse intestine.
  • This induction was significantly reduced by T2R38 siRNA and YM022 treatment.
  • PTC also enhanced the efflux activity of ABCB1, indicating increased transporter function.

Conclusions:

  • Gut ABCB1 expression and function are regulated by T2R signaling via CCK/gastrin pathways.
  • This T2R-mediated modulation of gut efflux transporters limits the absorption of bitter-tasting or toxic substances.

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