Figure 5. Thermogenic adipocytes promote reverse cholesterol transport without altering cholesterol efflux capacity of HDL.

Serum and HDL were prepared from wild-type C57BL/6J mice housed at thermoneutrality (mock), at 4 °C (cold) or treated with CL for 7 days. Peritoneal macrophages were pre-loaded with ³H-cholesterol and specific cholesterol efflux was induced (a) in the absence (control) or in the presence of 2% serum for the indicated time or (b) in the absence (IM=incubation medium) or in the presence of 2% serum or 50 μg ml⁻¹ HDL for 4 h at 37 °C. Values are mean±s.e.m. of n=3 independent experiments. *P<0.05, versus mock (Student's t-test). For metabolic turnover studies, HDL from untreated (mock-HDL) or CL-treated (CL-HDL) wild-type C57BL/6J mice were radiolabelled. After injection of ¹²⁵I-protein shell- and ³H-cholesterol oleoyl ether core-radiolabelled HDL, (c) plasma clearance and (d) liver uptake of ³H-cholesterol oleoyl ether were determined. Values are mean±s.e.m. (n=7 per group). In vivo RCT assay in thermoneutral (mock), CL-treated and cold-exposed (e–g) C57BL/6J and (h–j) E3L.CETP mice after the injection of peritoneal macrophages, ex vivo loaded with LDL and ³H-cholesterol. Radioactivity was determined 48 h after macrophage injection (e,h) in plasma and (f,i) in liver as well as (g,j) 24 h and 48 h after macrophage injection in faeces. Values are mean±s.e.m. (n=8–10 per group).*P<0.05, **P<0.01, ***P<0.001, versus mock (Student's t-test).