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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Atherosclerosis. 2015 Jan 30;239(2):364–374. doi: 10.1016/j.atherosclerosis.2015.01.013

Figure 1. Serum LDL-C and PCSK9 levels were inversely correlated in mice fed a HFD.

Figure 1

Male C57BL/6J mice fed a HFD (n=8) or a NCD (n=8) for three weeks were euthanized after a 4-h fast. Serum and liver samples were collected. (A) Serum TC and HDL-C of individual mouse were measured after three weeks on NCD or HFD. The concentrations of non-HDL-C were derived after subtraction of HDL-C from total cholesterol. (B, C) The profiles of lipoproteincholesterol and triglyceride of pooled mouse serum samples from HFD and NCD groups were analyzed using HPLC. (D) Hepatic TC and TG levels were measured in individual mouse liver samples. (E) Individual mouse serum insulin levels were quantified by a mouse/rat insulin ELISA kit. (F) Individual mouse serum PCSK9 levels were quantified by a mouse PCSK9 ELISA kit. (G) Real-time PCR analysis of mouse liver mRNA levels of indicated genes in HFD and NCD groups. (H) 50 μg of homogenate proteins of individual mouse liver samples were resolved by SDS-PAGE. LDLR and PCSK9 were detected by Western blot. The protein abundance of LDLR or PCSK9 was quantified with the Alpha View Software with normalization by signals of β-actin. Values are the mean ± SEM of 8 samples per group. *p < 0.05, **p < 0.01 and ***p < 0.001 as compared to NCD group.