Document Detail


Role of follistatin in promoting adipogenesis in women.
MedLine Citation:
PMID:  19470636     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CONTEXT: Follistatin is a glycoprotein that binds and neutralizes biological activities of TGFbeta superfamily members including activin and myostatin. We previously identified by expression profiling that follistatin levels in white adipose tissue (WAT) were regulated by obesity.
OBJECTIVE: The objective of the study was to elucidate the role of follistatin in human WAT and obesity.
DESIGN: We measured secreted follistatin protein from WAT biopsies and fat cells in vitro. We also quantified follistatin mRNA expression in sc and visceral WAT and in WAT-fractionated cells and related it to obesity status, body region, and cellular origin. We investigated the effects of follistatin on adipocyte differentiation of progenitor cells in vitro.
PARTICIPANTS: Women (n = 66) with a wide variation in body mass index were recruited by advertisement and from a clinic for weight-reduction therapy.
RESULTS: WAT secreted follistatin in vitro. Follistatin mRNA levels in sc but not visceral WAT were decreased in obesity and restored to nonobese levels after weight reduction. Follistatin mRNA levels were high in the stroma-vascular fraction of WAT and low in adipocytes. Recombinant follistatin treatment promoted adipogenic differentiation of progenitor cells and neutralized the inhibitory action of myostatin on differentiation in vitro. Moreover, activin and myostatin signaling receptors were detected in WAT and adipocytes.
CONCLUSION: Follistatin is a new adipokine important for adipogenesis. Down-regulated WAT expression of follistatin in obesity may counteract adiposity but could, by inhibiting adipogenesis, contribute to hypertrophic obesity (large fat cells) and insulin resistance.
Authors:
John N Flanagan; Kristina Linder; Niklas Mejhert; Elisabeth Dungner; Kerstin Wahlen; Pauline Decaunes; Mikael Rydén; Peyman Björklund; Stefan Arver; Shalender Bhasin; Anne Bouloumie; Peter Arner; Ingrid Dahlman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-26
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  94     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-08-06     Completed Date:  2009-08-25     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3003-9     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Activin Receptors, Type II / genetics
Adipogenesis*
Adipose Tissue, White / metabolism
Adult
Cell Differentiation
Cells, Cultured
Fatty Acid-Binding Proteins / genetics
Female
Follistatin / genetics,  physiology*
Humans
Mesenchymal Stromal Cells / cytology
Middle Aged
PPAR gamma / genetics
Protein-Serine-Threonine Kinases / genetics
RNA, Messenger / analysis
Receptors, Transforming Growth Factor beta / genetics
Grant Support
ID/Acronym/Agency:
R01 AG037193/AG/NIA NIH HHS; R01 DK078512/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/FABP4 protein, human; 0/Fatty Acid-Binding Proteins; 0/Follistatin; 0/PPAR gamma; 0/RNA, Messenger; 0/Receptors, Transforming Growth Factor beta; EC 2.7.1.11/TGF-beta type I receptor; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.30/Activin Receptors, Type II; EC 2.7.11.30/activin receptor type II-B
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