Searchable abstracts of presentations at key conferences on calcified tissues

ba0002is17 | Obesity as a bone disease: round table | ICCBH2013

Bone as an endocrine organ

Baldock Paul

Our understanding of skeletal biology has revealed bone as a tissue under complex regulatory control, with numerous systems influencing bone development and remodeling. In contrast, the regulatory output from bone tissue is very minimal. However, skeletal research is currently undergoing a period of marked expansion. One aspect in particular is the relationship between bone and fat metabolism. In addition to well-defined responses to weight bearing, emerging evidence indicates...

ba0002is17biog | Obesity as a bone disease: round table | ICCBH2013

Bone as an endocrine organ

Baldock Paul

Biographical DetailsPaul Baldock is Senior Research Fellow and Group Leader of the Bone Regulation Group, Neuroscience Research Program, Garvan Institute of Medical Research, Sydney, Australia. He completed his PhD in Human Physiology at the University of Adelaide in 2001 and since then has gone on to win several awards. His areas of interest are bone mass, neuropeptide Y, bone strength, ...

ba0005oc2.5 | Bone mass and bone strength Wnt signalling | ECTS2016

Is circulating sclerostin an endocrine modulator of bone mass?

Kulkarni Rishikesh , Schindeler Aaron , Croucher Peter , Little David , Baldock Paul

Mechanosenstitive osteocytes in bone supress the local production of sclerostin in response to mechanical loading, to increase osteoblast differentiation and bone mass. In addition, sclerostin is secreted from osteocytes into the circulation. Serum sclerostin has been shown to correlate with osteoporosis and low bone mass, however there is limited evidence by which to determine whether serum sclerostin is acting either a biomark...

ba0005p231 | Energy metabolism and bone, fat and bone | ECTS2016

Osteocalcin transgenic mice reveal aspects of the bone/glucose axis, as well as powerful suppression of ectopic osteocalcin protein production

Horsnell Harry , Wee Natalie , Kulkarni Rishikesh , Herzog Herbert , Baldock Paul

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...

ba0003oc1.6 | Phosphate metabolism, fracture repair and osteoarthritis | ECTS2014

The role of neuropeptide Y Y1 receptor signalling in fracture healing

Sousa Daniela M , McDonald Michelle M , Mikulec Kathy , Peacock Lauren , Little David G , Herzog Herbert , Lamghari Meriem , Baldock Paul A

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...