An infection of human adenovirus 31 affects the differentiation of preadipocytes into fat cells, its metabolic profile and fat accumulation
The primary issue undertaken in this study was to test the hypothesis that preadipocytes would have intrinsically elevated propensity to differentiate into mature adipocytes due to HAdV31 infection. To prove that, the metabolic and molecular mechanisms responsible for HAdV31‐induced adipogenesis wer...
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Published in | Journal of medical virology Vol. 88; no. 3; pp. 400 - 407 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.03.2016
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The primary issue undertaken in this study was to test the hypothesis that preadipocytes would have intrinsically elevated propensity to differentiate into mature adipocytes due to HAdV31 infection. To prove that, the metabolic and molecular mechanisms responsible for HAdV31‐induced adipogenesis were examined. 3T3L1 cells (mouse embryonic fibroblast, adipose like cell line) were used as a surrogate model to analyze an increased proliferation, differentiation, and maturation of preadipocytes infected with human adenovirus. An expression of E4orf1, C/EBP‐β, PPAR‐γ, GAPDH, aP2, LEP, and fatty acid synthase genes, intracellular lipid accumulation as well as cytokine release from the fat cells were assessed. Data showed that HAdV31 increased an expression of C/EBP‐β and PPAR‐γ genes leading to an enhanced differentiation of preadipocytes into fat cells. Besides, overexpression of GAPDH and fatty acid synthase, and decreased expression of leptin caused an increased accumulation of intracellular lipids. Secretion of TNF‐α and IL‐6 from HAdV31‐infected cells was strongly decreased, leading to unlimited virus replication. The results obtained from this study provided the evidences that HAdV31, likewise previously documented HAdV36, is a subsequent human adenovirus affecting the differentiation and lipid accumulation of 3T3L1 cells. J. Med. Virol. 88:400–407, 2016. © 2015 Wiley Periodicals, Inc. |
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Bibliography: | ArticleID:JMV24362 ark:/67375/WNG-DS5D7TLN-4 istex:14FE4B9916E411888897754E23F24A317404FB74 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0146-6615 1096-9071 |
DOI: | 10.1002/jmv.24362 |