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A novel anti‐lipogenic regulator aborts adipogenic cascade of preadipocyte differentiation
Author(s) -
Rathod Miloni A,
Rogers Pamela M,
Dhurandhar Nikhil V
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a702-c
Subject(s) - adipogenesis , endocrinology , medicine , adipocyte , biology , gene expression , per1 , chemistry , microbiology and biotechnology , gene , adipose tissue , biochemistry , clock
Experimental infection with human adenovirus Ad‐36, not Ad‐2, increases adiposity in animals and natural infection shows association with human obesity. In rodent and human adipocyte progenitor cultures, Ad‐36 induces but Ad‐2 reduces lipid accumulation despite viral gene expression. To identify the mechanism for anti‐lipogenic effect, the effects of Ad‐2 on time course of adipogenic gene expression cascade up to 7 days post infection was determined in absence or presence of adipogenic inducers‐ methyl isobutyl xanthine, dexamethasone and insulin (MDI). Ad‐36 was used as an adipogenic positive control. Ad‐2 infected groups had significantly lower lipid accumulation even in the presence of MDI. By acting downstream of C/EBPβ, Ad‐2 appears to abort the adipogenic gene expression cascade initiated by MDI and thus inhibit lipid accumulation. The findings provide novel insight in control of down regulation of cellular pathways of adipogenesis. Funded by NIH R‐01 DK066164. 1 Changes in gene expression and lipid accumulation by Ad‐36 and Ad‐2 compared to uninfected control groups, in 3T3‐L1 preadipocytes expressing CAR‐receptor for efficient viral entry. p < .05 for all changes noted. ND: no difference vs uninfected control.