Niemann-Pick C1 protects against atherosclerosis in mice via regulation of macrophage intracellular cholesterol trafficking
J. Clin. Invest. Jessie R. Zhang, et al. 118:2281 doi:10.1172/JCI32561 [Go to this article.]

Figure 3
Lipoprotein metabolism studies in MϕNpc1^+/+ and MϕNpc1^–/– mice fed an atherogenic diet for 10 weeks. (A) Body weight. (B) TG production. Fasting TG levels were determined at time 0. Mice were injected with Triton WR 1339 to inhibit systemic lipolysis or with PBS control, and venipuncture was performed at 30, 60, and 120 minutes. (C) VLDL clearance. Mice were injected with ¹²⁵I-VLDL, and blood was collected 0–240 minutes after injection. The amount of ¹²⁵I-VLDL remaining in plasma at each time point was expressed as a percentage relative to the ¹²⁵I-radioactivity in the plasma 1 minute after initial injection. (D) Liver tissue cholesterol content (n = 8–9 per genotype). (E) Cholesterol content of Kupffer cell fractions isolated from the liver. Fractions from 2 mice per genotype were pooled, lipids were extracted, and cholesterol was measured by GC/MS. FC, free cholesterol; CE, cholesterol ester. For all experiments shown, data are mean ± SEM of triplicate determinations and are representative of 2 independent experiments. *P < 0.05 versus MϕNpc1^+/+.