PMID- 24060147
OWN - NLM
STAT- MEDLINE
DCOM- 20140908
LR  - 20190911
IS  - 1873-5592 (Electronic)
IS  - 1389-4501 (Linking)
VI  - 14
IP  - 14
DP  - 2013 Dec
TI  - Osteoporosis and its association with non-gonadal hormones involved in 
      hypertension, adiposity and hyperglycaemia.
PG  - 1694-706
AB  - Osteoporosis is a high-prevalence disease, particularly in developed countries, 
      and results in high costs both to the individual and to society through 
      associated fragility fractures. There is an urgent need for identification of 
      novel drug targets and development of new anti-osteoporotic agents. Between 30 
      and 80% of osteoporotic fractures cannot be prevented despite current treatments 
      achieving relative fracture risk reduction of up to 20%, 50%, and 70% for 
      non-vertebral, hip and spine fractures, respectively. Traditionally, the decline 
      in gonadal hormones has been studied as the sole hormonal determinant for the 
      loss of bone mineral density in osteoporosis. However, recent studies have 
      identified receptors for numerous non-gonadal hormones such as PTH, angiotensin 
      II, leptin, adiponectin, insulin and insulin-like growth factor-1 on the 
      osteoblast lineage cells that directly regulate bone turnover. These hormones are 
      also involved in the pathogenesis of metabolic syndrome risk factors, 
      particularly hypertension, type-II diabetes and obesity. By activating their 
      respective receptors on osteoblastic lineage cells, these hormones appear to act 
      through a common mechanism by down-regulating receptors for activation of nuclear 
      factor kappa B ligand (RANKL) and up-regulating osteoprotegerin (OPG) with 
      inverse responses for adiponectin. Receptors for amylin, gastric inhibitory 
      polypeptide and ghrelin and have also been identified on the osteoblast lineage 
      cells although the roles of these receptors in bone turnover are controversial or 
      poorly studied. Moreover, bone turnover may be independently regulated by 
      modulation of osteoclast-osteoblast function and bone marrow adiposity. Leptin 
      appears to be the only hormone that is a known regulator of both bone 
      mineralisation and bone adiposity.
FAU - Poudyal, Hemant
AU  - Poudyal H
FAU - Brown, Lindsay
AU  - Brown L
AD  - School of Health, Nursing and Midwifery, University of Southern Queensland, 
      Toowoomba, QLD 4350, Australia. Lindsay.Brown@usq.edu.au.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Drug Targets
JT  - Current drug targets
JID - 100960531
RN  - 0 (Hormones)
RN  - 0 (Leptin)
RN  - 0 (Parathyroid Hormone)
RN  - 0 (RANK Ligand)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (Receptors, Cell Surface)
SB  - IM
MH  - *Adiposity
MH  - Animals
MH  - Bone Remodeling
MH  - Hormones/*metabolism
MH  - Humans
MH  - Hyperglycemia/etiology/*metabolism
MH  - Hypertension/etiology/*metabolism
MH  - Leptin/metabolism
MH  - Osteoclasts/metabolism/pathology
MH  - Osteoporosis/complications/*metabolism/pathology
MH  - Parathyroid Hormone/metabolism
MH  - RANK Ligand/metabolism
MH  - Receptor Activator of Nuclear Factor-kappa B/metabolism
MH  - Receptors, Cell Surface/*metabolism
MH  - Signal Transduction
EDAT- 2013/09/26 06:00
MHDA- 2014/09/10 06:00
CRDT- 2013/09/25 06:00
PHST- 2013/08/11 00:00 [received]
PHST- 2013/09/13 00:00 [revised]
PHST- 2013/09/16 00:00 [accepted]
PHST- 2013/09/25 06:00 [entrez]
PHST- 2013/09/26 06:00 [pubmed]
PHST- 2014/09/10 06:00 [medline]
AID - CDT-EPUB-56231 [pii]
AID - 10.2174/1389450119999990001 [doi]
PST - ppublish
SO  - Curr Drug Targets. 2013 Dec;14(14):1694-706. doi: 10.2174/1389450119999990001.