Document Detail


PPARgamma-independent increase in glucose uptake and adiponectin abundance in fat cells.
MedLine Citation:
PMID:  21791563     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although thiazolidinediones (TZD) effectively improve hyperglycemia and increase adiponectin, a proinsulin-sensitizing adipokine, they also increase adipogenesis via peroxisome proliferator-activated receptor (PPAR)γ induction, which may be undesirable. Recent safety concerns about some TZD have prompted the search for next generation agents that can enhance glycemic control and adiponectin independent of PPARγ or adipogenesis. Reminiscent of TZD action, a human adenovirus, adenovirus 36 (Ad36), up-regulates PPARγ, induces adipogenesis, and improves systemic glycemic control in vivo. We determined whether this effect of Ad36 requires PPARγ and/or adipogenesis. Glucose uptake and relevant cell signaling were determined in mock-infected or human adenoviruses Ad36 or Ad2-infected cell types under the following conditions: 1) undifferentiated human-adipose-tissue-derived stem cells (hASC), 2) hASC differentiated as adipocytes, 3) hASC in presence or absence of a PPARγ inhibitor, 4) NIH/3T3 that have impaired PPARγ expression, and 5) PPARγ-knockout mouse embryonic fibroblasts. Mouse embryonic fibroblasts with intact PPARγ served as a positive control. Additionally, to determine natural Ad36 infection, human sera were screened for Ad36 antibodies. In undifferentiated or differentiated hASC, or despite the inhibition, down-regulation, or the absence of PPARγ, Ad36 significantly enhanced glucose uptake and PPARγ, adiponectin, glucose transporter 4, and glucose transporter 1 protein abundance, compared with mock or Ad2-infected cells. This indicated that Ad36 up-regulates glucose uptake and adiponectin secretion independent of adipogenesis or without recruiting PPARγ. In humans, natural Ad36 infection predicted greater adiponectin levels, suggesting a human relevance of these effects. In conclusion, Ad36 provides a novel template to metabolically remodel human adipose tissue to enhance glycemic control without the concomitant increase in adiposity or PPARγ induction associated with TZD actions.
Authors:
Olga Dubuisson; Emily J Dhurandhar; Rashmi Krishnapuram; Heather Kirk-Ballard; Alok K Gupta; Vijay Hegde; Elizabeth Floyd; Jeffrey M Gimble; Nikhil V Dhurandhar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-07-26
Journal Detail:
Title:  Endocrinology     Volume:  152     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-22     Completed Date:  2011-11-10     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3648-60     Citation Subset:  AIM; IM    
Affiliation:
Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808, USA.
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MeSH Terms
Descriptor/Qualifier:
3T3-L1 Cells
Adipocytes / metabolism*
Adipogenesis
Adiponectin / metabolism*
Aged
Anilides / pharmacology
Animals
Cells, Cultured
Female
Glucose / metabolism*
Humans
Male
Mice
Middle Aged
NIH 3T3 Cells
PPAR gamma / antagonists & inhibitors,  physiology*
Grant Support
ID/Acronym/Agency:
1P30 DK072476/DK/NIDDK NIH HHS; 1P30-DK072476/DK/NIDDK NIH HHS; P20-RR021945/RR/NCRR NIH HHS; R-01 DK066164/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/2-chloro-5-nitrobenzanilide; 0/Adiponectin; 0/Anilides; 0/PPAR gamma; 50-99-7/Glucose
Comments/Corrections

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


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