Abstract
BACKGROUND AND PURPOSE-: Adipose inflammation is crucial to the pathogenesis of metabolic disorders. This study aimed at identify the effects of stearoyl-CoA desaturase-1 (SCD1) on the inflammatory response of a paracrine network involving adipocytes, macrophages, and endothelial cells. METHODS AND RESULTS-: Loss of SCD1 in both genetic (Agouti) and diet-induced obesity (high-fat diet) mouse models prevented inflammation in white adipose tissue and improved its basal insulin signaling. In SCD1-deficient mice, white adipose tissue exhibited lower inflammation, with a reduced response to lipopolysaccharide in isolated adipocytes, but not in peritoneal macrophages. Mimicking the in vivo paracrine regulation of white adipose tissue inflammation, SCD1-deficient adipocyte-conditioned medium attenuated the induction of tumor necrosis factor (TNF) α/interleukin 1β gene expression in RAW264.7 macrophages and reduced the adhesion response in endothelial cells. We further demonstrated that the adipocyte-derived oleate (18:1n9), but not palmitoleate (16:1n7), mediated the inflammation in macrophages and adhesion responses in endothelial cells. CONCLUSIONS-: Loss of SCD1 attenuates adipocyte inflammation and its paracrine regulation of inflammation in macrophages and endothelial cells. The reduced oleate level is linked to the inflammation-modulating effects of SCD1 deficiency.
Original language | English (US) |
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Pages (from-to) | 31-38 |
Number of pages | 8 |
Journal | Arteriosclerosis, thrombosis, and vascular biology |
Volume | 30 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2010 |
Externally published | Yes |
Keywords
- Adipocyte
- Endothelial cells
- Inflammation
- Macrophage
- Oleate
- Palmitoleate
- SCD1
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine