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Peptide YY is critical for acylethanolamine receptor Gpr119-induced activation of gastrointestinal mucosal responses


Peptide YY (PYY) is released following food intake and regulates intestinal function and glucose homeostasis, but the mechanisms underpinning these processes are unclear. Enteroendocrine L cells contain PYY and express the acylethanolamine receptor, Gpr119. Here, we show that Gpr119 activation inhibited epithelial electrolyte secretion in human and mouse colon in a glucose-sensitive manner. Endogenous PYY selectively mediated these effects, since PYY(-/-) mice showed no Gpr119 response, but responses were observed in NPY(-/-) mice. Importantly, Gpr119 responses in wild-type (WT) mouse tissue and human colon were abolished by Y(1) receptor antagonism, but were not enhanced by dipeptidylpeptidase IV blockade, indicating that PYY processing to PYY(3-36) was not important. In addition, Gpr119 agonism reduced glycemic excursions after oral glucose delivery to WT mice but not PYY(-/-) mice. Taken together, these data demonstrate a previously unrecognized role of PYY in mediating intestinal Gpr119 activity and an associated function in controlling glucose tolerance.

Type Journal
ISBN 1932-7420 (Electronic) 1550-4131 (Linking)
Authors Cox, H. M.; Tough, I. R.; Woolston, A. M.; Zhang, L.; Nguyen, A. D.; Sainsbury, A.; Herzog, H.;
Garvan Authors Prof Herbert Herzog , Dr Lei Zhang
Publisher Name CELL METAB
Published Date 2010-01-01 00:00:00
Published Volume 11
Published Issue 6
Published Pages 532-42
Status Published In-print
OpenAccess Link Cox Cell Metab.pdf