Bone Abstracts

see P231....

Rationale: Mice deficient in osteocalcin show an impaired glucose tolerance, however, the exact mechanism involved have yet to be fully elucidated. We aimed to overexpress osteocalcin to determine its effect on glucose homeostasis and explore the signalling pathway involved. We wished to expand upon previous preliminary data suggesting that this pathway involve neuropeptide Y (NPY) signalling.Objective: To analyse the in vivo and in vitro</e...

Recent studies have demonstrated that the global or osteoblast-specific deletion of neuropeptide Y Y1 receptor (Y1R), as well as the pharmacological blockade of Y1R, leads to pronounced anabolic effects in bone metabolism. This suggests that anti-Y1R drug therapy might have clinical applications for the prevention/recovery of bone loss occurring in osteoporosis. Given the high fracture incidence in this target population, it remained...

see P194....

Neuropeptide Y Y1 receptor (Y1R) signalling has been shown to play a key role in bone homeostasis, emerging as a novel therapeutic target in bone diseases. Y1R knockout mice (Y1−/−) display a high-bone mass phenotype that has been mainly attributed to increased osteoblast activity. Nevertheless, the Y1R regulatory role on osteoclastogenesis and matrix resorption remains largely unknown. To clarify th...