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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Biochim Biophys Acta Mol Cell Biol Lipids. 2018 Dec 20;1864(3):358–371. doi: 10.1016/j.bbalip.2018.12.012

Fig. 6.

Fig. 6.

Effects of knocking down hepatic ACSL1 in mice fed a NCD. Male C57BL/6J mice fed a NCD were injected with Ad-shAcsl1 or Ad-shU6-C. After 11-days of adenoviral injection, mice were sacrificed and serum and livers were isolated at the termination. All data are mean ± SEM of 6 mice per group.

(A) Western blot analysis of hepatic ACSL1 protein and β-actin levels. The protein abundance of ACSL1 was quantified and normalized with signals of P-actin using Alpha View Software.

(B) Real-time PCR was conducted to determine the relative expression levels of ACSL isoform mRNAs after normalization with GAPDH mRNA levels.

(C) Total ACSL enzymatic activity in 4 μg of liver homogenate using [3H] labeled PA, [3H] labeled OA and [3H] labeled AA as substrates.

(D) Serum TC.

(E) Serum FC.

(F) Serum triglycerides.

(G) Liver TC.

(H) Liver FC.

(I) Liver TG.

(J) Liver total BA amounts.

(K, L) Real-time PCR measurement of hepatic mRNA levels of indicated genes in BA synthesis and cholesterol metabolism.

In A–L, Significance was determined by Student’s t-test. n = 6 mice per group. *p < 0.05, **p < 0.01, and ***p < 0.001.