These findings demonstrate that PYY acts as a negative regulator of osteoblastic bone formation, implicating increased PYY levels in the pathogenesis of bone loss during anorexia or following bariatric surgery.
Anorectic response to the trichothecene T-2 toxin correspond to plasma elevations of the satiety hormone glucose-dependent insulinotropic polypeptide and peptide YY3-36.
The intraperitoneal bolus administration of PYY<sub>3-36</sub> and a 12-amino acid PYY analogue, benzoyl-[Cha<sup>27,28,36</sup>,Aib<sup>31</sup>]PYY<sub>25-36</sub> (<b>1</b>), showed similar anorectic activity by activating the Y2 receptor (Y2R).
In normal-weight and obese human subjects, high-protein intake induced the greatest release of the anorectic hormone peptide YY (PYY) and the most pronounced satiety.