| First Author | Wortley KE | Year | 2007 |
| Journal | Gastroenterology | Volume | 133 |
| Issue | 5 | Pages | 1534-43 |
| PubMed ID | 17920065 | Mgi Jnum | J:130105 |
| Mgi Id | MGI:3770742 | Doi | 10.1053/j.gastro.2007.08.024 |
| Citation | Wortley KE, et al. (2007) Peptide YY regulates bone turnover in rodents. Gastroenterology 133(5):1534-43 |
| abstractText | BACKGROUND & AIMS: Peptide YY (PYY) and pancreatic polypeptide (PPY) are members of the neuropeptide Y peptide family. The neuropeptide Y receptor signaling pathway has been implicated in a number of physiologic processes, including the regulation of energy balance and bone mass. To investigate the contribution of endogenous PYY and PPY to these processes, we generated both Pyy- and Ppy-deficient mice. METHODS: Pyy(-/-) and Ppy(-/-) mice and their respective wild-type littermates were studied from 8 weeks to 9 months of age. Food intake, metabolic parameters, and locomotor activity were monitored using indirect calorimetry. Body composition and bone parameters were analyzed using dual energy x-ray absorptiometry, histomorphometry, and vertebral compression testing. RESULTS: Studies in these mice showed an osteopenic phenotype specific to the Pyy-deficient line, which included a reduction in trabecular bone mass and a functional deficit in bone strength. Furthermore, female Pyy(-/-) mice showed a greater sensitivity to ovariectomy-induced bone loss compared with wild-type littermates. No food intake or metabolic phenotype was apparent in male or female Pyy(-/-) mice on standard chow. However, female Pyy(-/-) mice on a high-fat diet showed a greater propensity to gain body weight and adiposity. No metabolic or osteopenic phenotype was observed in Ppy-deficient mice. CONCLUSIONS: These results indicate that endogenous PYY plays a critical role in regulating bone mass. In comparison, its role in regulating body weight is minor and is confined to situations of high-fat feeding. |
