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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Cell Metab. 2020 Nov 4;32(6):1012–1027.e7. doi: 10.1016/j.cmet.2020.10.010

Figure 6. The fasting-stimulated mitochondrial localization of ACSL1 is impaired in LTKO liver.

Figure 6.

(A) The protein levels of ACSL1, ACSL4, and TBK1 in liver tissues from NCD-fed flox mice or LTKO mice. n = 4–8 mice per group. (B) Quantified levels of ACSL1 and ACSL4 expression in livers. (C) The expression of ACSL1 and TBK1 in mitochondrial and microsomal fraction of liver tissues from NCD-fed flox or LTKO mice. Ponceau band was used for loading control. n = 5 mice per group. (D) Quantified level of ACSL1 (normalized with ponceau band) in mitochondria. (E) Quantified level of ACSL1 (normalized with ponceau band) in microsome. (F) Quantified level of TBK1 (normalized with ponceau band) in mitochondria of flox mice. (G) Quantified level of TBK1 (normalized with ponceau band) in microsome of flox mice. (H-J) Re-esterification activity in primary hepatocytes from flox or LTKO mice upon [U-14C] palmitate. n = 3 replicates per group. (H) Autoradiography image for triglyceride (TG), diacylglyceride (DG) and polar lipid (PL). (I) Quantified band density of TG. (J) Quantified ratio of TG/PL. For data in (B), (D), and (E), *p < 0.05, **p < 0.01 for flox compared to LTKO in same feeding condition, #p < 0.05, ##p < 0.01 for fed compared to fasting in each genotype, two-way ANOVA followed Holm-Sidak’s multiple comparisons test was analyzed. Student t test was analyzed for (F), (G), (I), and (J). All data in the figure are shown as the mean ± SEM. See also Figure S6A and S6B.