Document Detail


Pharmacological interference with transcriptional control of osteoblasts: a possible role for leptin and fatty acids in maintaining bone strength and body lean mass.
MedLine Citation:
PMID:  11254890     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Osteoblasts pass through a sequence of events controlled by hormones and transcriptional factors ensuring proper development of phenotype and functional properties until the osteoblast enter the osteocyte phenotype and/or undergo apoptosis. During its life cycle, the osteoblasts proliferate, deposit matrix proteins and mineralize it until they turn into osteocytes believed to constitute a mechanosensor mesh giving feed-back to the osteoblast to initiate bone modeling or remodeling necessary for the making or remaking of proper bone architecture and strength. It appears that several factors common to osteoblast and adipocyte differentiation determine their entry into different functional stages. Such factors are insulin, growth hormone (GH), insulin-like growth factor type I (IGF-I), transforming growth factor beta (TGFbeta), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), cytokines (e.g. interleukins, interferon and tumor necrosis factor alpha (TNF alpha), bone morphogenetic proteins (BMPs), glucocorticoids, retinoic acid (RA), prostaglandins and cAMP-elevating hormones. The focus of this article is to review the effects of leptin on bone cells and bone turnover, the peroxisome proliferator-activated receptors (PPARs) in the regulation of bone and fat cell differentiation, hormones and fatty acids on the orchestration of osteoblast and adipocyte derived regulatory signals, and mechanostimulation of bone on the mechanisms by which the above mentioned factors modulate osteoblast and adipocyte function. The hypothesis or concept is that prescription of a certain treatment regimen to correct bone turnover, without attempting to assess how hormonal homeostasis, nutritional factors and physical exercise may interact locally, will remain far from optimal, and may even prove detrimental to the patient's health condition.
Authors:
J O Gordeladze; J E Reseland; C A Drevon
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current pharmaceutical design     Volume:  7     ISSN:  1381-6128     ISO Abbreviation:  Curr. Pharm. Des.     Publication Date:  2001 Mar 
Date Detail:
Created Date:  2001-03-20     Completed Date:  2001-05-03     Revised Date:  2006-02-27    
Medline Journal Info:
Nlm Unique ID:  9602487     Medline TA:  Curr Pharm Des     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  275-90     Citation Subset:  IM    
Affiliation:
Institute of Medical Biochemistry, University of Oslo, P.O. Box 1112, Blindern, Oslo, 0317, Norway.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / physiology
Animals
Apoptosis
Body Composition*
Bone Density*
Cell Differentiation
Cell Division
Cell Lineage
Fatty Acids / physiology*
Gene Expression Regulation
Humans
Interleukin-6 / physiology
Leptin / physiology*
Osteoblasts / physiology*
Receptors, Cytoplasmic and Nuclear / physiology
Stromal Cells / physiology
Transcription Factors / physiology
Transcription, Genetic*
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Interleukin-6; 0/Leptin; 0/Receptors, Cytoplasmic and Nuclear; 0/Transcription Factors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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