Abstract
Brown and beige adipocytes combust nutrients for thermogenesis and through their metabolic activity decrease pro-atherogenic remnant lipoproteins in hyperlipidemic mice. However, whether the activation of thermogenic adipocytes affects the metabolism and anti-atherogenic properties of high-density lipoproteins (HDL) is unknown. Here, we report a reduction in atherosclerosis in response to pharmacological stimulation of thermogenesis linked to increased HDL levels in APOE(star)3-Leiden. CETP mice. Both cold-induced and pharmacological thermogenic activation enhances HDL remodelling, which is associated with specific lipidomic changes in mouse and human HDL. Furthermore, thermogenic stimulation promotes HDL-cholesterol clearance and increases macrophage-to-faeces reverse cholesterol transport in mice. Mechanistically, we show that intravascular lipolysis by adipocyte lipoprotein lipase and hepatic uptake of HDL by scavenger receptor B-I are the driving forces of HDL-cholesterol disposal in liver. Our findings corroborate the notion that high metabolic activity of thermogenic adipocytes confers atheroprotective properties via increased systemic cholesterol flux through the HDL compartment.
Original language | English |
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Article number | 15010 |
Number of pages | 10 |
Journal | Nature Communications |
Volume | 8 |
DOIs | |
Publication status | Published - 19 Apr 2017 |
Keywords
- BROWN ADIPOSE-TISSUE
- HIGH-DENSITY-LIPOPROTEIN
- TYPE-2 DIABETES-MELLITUS
- APOLIPOPROTEIN-A-I
- CARDIOVASCULAR-DISEASE
- SCAVENGER RECEPTOR
- COLD-EXPOSURE
- ADAPTIVE THERMOGENESIS
- CELLULAR CHOLESTEROL
- ENERGY-EXPENDITURE