Document Detail


Regional differences in cellular mechanisms of adipose tissue gain with overfeeding.
MedLine Citation:
PMID:  20921416     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Body fat distribution is an important predictor of the metabolic consequences of obesity, but the cellular mechanisms regulating regional fat accumulation are unknown. We assessed the changes in adipocyte size (photomicrographs) and number in response to overfeeding in upper- and lower-body s.c. fat depots of 28 healthy, normal weight adults (15 men) age 29 ± 2 y. We analyzed how these changes relate to regional fat gain (dual energy X-ray absorptiometry and computed tomography) and baseline preadipocyte proliferation, differentiation [peroxisome proliferator-activated receptor-γ2 (PPARγ2) and CCAAT/enhancer binding protein-α (C/EBPα) mRNA]), and apoptotic response to TNF-α. Fat mass increased by 1.9 ± 0.2 kg in the upper body and 1.6 ± 0.1 kg in the lower body. Average abdominal s.c. adipocyte size increased by 0.16 ± 0.06 μg lipid per cell and correlated with relative upper-body fat gain (r = 0.74, P < 0.0001). However, lower-body fat responded to overfeeding by fat-cell hyperplasia, with adipocyte number increasing by 2.6 ± 0.9 × 10(9) cells (P < 0.01). We found no depot-differences in preadipocyte replication or apoptosis that would explain lower-body adipocyte hyperplasia and abdominal s.c. adipocyte hypertrophy. However, baseline PPARγ2 and C/EBPα mRNA were higher in abdominal than femoral s.c. preadipocytes (P < 0.005 and P < 0.03, respectively), consistent with the ability of abdominal s.c. adipocytes to achieve a larger size. Inherent differences in preadipocyte cell dynamics may contribute to the distinct responses of different fat depots to overfeeding, and fat-cell number increases in certain depots in adults after only 8 wk of increased food intake.
Authors:
Yourka D Tchoukalova; Susanne B Votruba; Tamara Tchkonia; Nino Giorgadze; James L Kirkland; Michael D Jensen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't     Date:  2010-10-04
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  107     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-20     Completed Date:  2010-11-22     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  18226-31     Citation Subset:  IM    
Affiliation:
Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA.
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MeSH Terms
Descriptor/Qualifier:
Absorptiometry, Photon
Adipocytes / metabolism
Adipose Tissue / cytology,  metabolism*
Adult
Body Composition
CCAAT-Enhancer-Binding Protein-alpha / genetics,  metabolism
Energy Intake*
Female
Humans
Male
PPAR gamma / genetics,  metabolism
Tomography, X-Ray Computed
Tumor Necrosis Factor-alpha / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
AG13925/AG/NIA NIH HHS; DK45343/DK/NIDDK NIH HHS; DK50456/DK/NIDDK NIH HHS; R01 AG013925-13/AG/NIA NIH HHS; R01 DK045343-20/DK/NIDDK NIH HHS; RR00585/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/CCAAT-Enhancer-Binding Protein-alpha; 0/PPAR gamma; 0/Tumor Necrosis Factor-alpha
Comments/Corrections

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


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