Preadipocyte response and impairment of differentiation in an inflammatory environment

Recent reports suggest the potential role of toll-like receptor 4 (TLR4) in initiation of inflammatory responses and fatty acid-induced insulin resistance. We describe here the synthesis of pro-inflammatory products in 3T3-L1 preadipocyte cell line after stimulation with lipopolysaccharide (LPS), a...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-05, Vol.356 (3), p.662-667
Main Authors: Poulain-Godefroy, Odile, Froguel, Philippe
Format: Article
Language:English
Subjects:
3T3-L1
3T3-L1 Cells
Adipocyte
Adipocytes
Adipocytes - physiology
Adipokine
Animals
Cell Differentiation
Cell Differentiation - physiology
Chemokines
Chemokines - biosynthesis
Cyclooxygenase 2
Cyclooxygenase 2 - biosynthesis
Cytokines
Cytokines - biosynthesis
Differentiation
Gene Expression Regulation
Gene Expression Regulation - drug effects
Genetics
Human genetics
Inflammation
Inflammation - physiopathology
Life Sciences
Lipopolysaccharides
Lipopolysaccharides - pharmacology
Mice
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type II - biosynthesis
Obesity
TLR4
Toll-Like Receptor 4
Toll-Like Receptor 4 - physiology
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Summary:Recent reports suggest the potential role of toll-like receptor 4 (TLR4) in initiation of inflammatory responses and fatty acid-induced insulin resistance. We describe here the synthesis of pro-inflammatory products in 3T3-L1 preadipocyte cell line after stimulation with lipopolysaccharide (LPS), a TLR4 agonist. Expression profiles of mRNA coding for IL6, CCL2, CCL5, CCL11, NOS2, and PTGS2 demonstrated a higher responsiveness to LPS of these transcripts in preadipocytes than in fully differentiated adipocytes, confirming inflammatory features of preadipocytes. IL6, CCL2, CCL5 and CCL11 were secreted in 3T3-L1 supernatants within 4 h after LPS stimulation. In addition, continuous exposure to LPS during adipocyte differentiation impaired this process as was demonstrated by analysis of mRNA profiles of lipogenesis enzymes (FABP4, GPD1, LPL), adipokines (adiponectin, resistin, visfatin, leptin), and of the transcription factor PPARĪ³. This suggests that toll-like receptor mediated activation could regulate maintenance of preadipocyte status, and inflammatory environment encountered in inflamed white adipose tissue.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.03.053