Energy Balance, Myostatin, and GILZ: Factors Regulating Adipocyte Differentiation in Belly and Bone.

Hdl Handle:
http://hdl.handle.net/10675.2/55
Title:
Energy Balance, Myostatin, and GILZ: Factors Regulating Adipocyte Differentiation in Belly and Bone.
Authors:
Shi, Xing-Ming; Hamrick, Mark; Isales, Carlos M
Abstract:
Peroxisome proliferator-activated receptor gamma (PPAR-gamma) belongs to the nuclear hormone receptor subfamily of transcription factors. PPARs are expressed in key target tissues such as liver, fat, and muscle and thus they play a major role in the regulation of energy balance. Because of PPAR-gamma's role in energy balance, signals originating from the gut (e.g., GIP), fat (e.g., leptin), muscle (e.g., myostatin), or bone (e.g., GILZ) can in turn modulate PPAR expression and/or function. Of the two PPAR-gamma isoforms, PPAR-gamma2 is the key regulator of adipogenesis and also plays a role in bone development. Activation of this receptor favors adipocyte differentiation of mesenchymal stem cells, while inhibition of PPAR-gamma2 expression shifts the commitment towards the osteoblastogenic pathway. Clinically, activation of this receptor by antidiabetic agents of the thiazolidinedione class results in lower bone mass and increased fracture rates. We propose that inhibition of PPAR-gamma2 expression in mesenchymal stem cells by use of some of the hormones/factors mentioned above may be a useful therapeutic strategy to favor bone formation.
Citation:
PPAR Res. 2007 Nov 25; 2007:92501
Issue Date:
29-Feb-2008
URI:
http://hdl.handle.net/10675.2/55
DOI:
10.1155/2007/92501
PubMed ID:
18309369
PubMed Central ID:
PMC2246068
Type:
Journal Article
ISSN:
1687-4757
Appears in Collections:
Institute of Molecular Medicine and Genetics: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorShi, Xing-Mingen_US
dc.contributor.authorHamrick, Marken_US
dc.contributor.authorIsales, Carlos Men_US
dc.date.accessioned2010-09-24T21:26:48Z-
dc.date.available2010-09-24T21:26:48Z-
dc.date.issued2008-02-29en_US
dc.identifier.citationPPAR Res. 2007 Nov 25; 2007:92501en_US
dc.identifier.issn1687-4757en_US
dc.identifier.pmid18309369en_US
dc.identifier.doi10.1155/2007/92501en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/55-
dc.description.abstractPeroxisome proliferator-activated receptor gamma (PPAR-gamma) belongs to the nuclear hormone receptor subfamily of transcription factors. PPARs are expressed in key target tissues such as liver, fat, and muscle and thus they play a major role in the regulation of energy balance. Because of PPAR-gamma's role in energy balance, signals originating from the gut (e.g., GIP), fat (e.g., leptin), muscle (e.g., myostatin), or bone (e.g., GILZ) can in turn modulate PPAR expression and/or function. Of the two PPAR-gamma isoforms, PPAR-gamma2 is the key regulator of adipogenesis and also plays a role in bone development. Activation of this receptor favors adipocyte differentiation of mesenchymal stem cells, while inhibition of PPAR-gamma2 expression shifts the commitment towards the osteoblastogenic pathway. Clinically, activation of this receptor by antidiabetic agents of the thiazolidinedione class results in lower bone mass and increased fracture rates. We propose that inhibition of PPAR-gamma2 expression in mesenchymal stem cells by use of some of the hormones/factors mentioned above may be a useful therapeutic strategy to favor bone formation.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.titleEnergy Balance, Myostatin, and GILZ: Factors Regulating Adipocyte Differentiation in Belly and Bone.en_US
dc.typeJournal Articleen_US
dc.identifier.pmcidPMC2246068en_US
dc.contributor.corporatenameInstitute of Molecular Medicine and Geneticsen_US
dc.contributor.corporatenameDepartment of Pathologyen_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomyen_US
dc.contributor.corporatenameDepartment of Orthopaedic Surgeryen_US
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