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Open Access Green as soon as Postprint is submitted to ZB.
Peptide YY regulates bone turnover in rodents.
Gastroenterology 133, 1534-1543 (2007)
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.
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Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2007
HGF-reported in Year
2007
ISSN (print) / ISBN
0016-5085
e-ISSN
1528-0012
Journal
Gastroenterology
Quellenangaben
Volume: 133,
Issue: 5,
Pages: 1534-1543
Publisher
Elsevier
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
PubMed ID
17920065
Erfassungsdatum
2020-02-24