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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 3. Loss of TBK1 suppresses fasting-induced fatty acid oxidation in liver.

Figure 3.

(A-C) mRNA expression of fatty acid uptake-related genes (A), lipogenesis genes (B), and fatty acid oxidation genes (C) in the liver tissues from HFD-fed flox and LTKO mice in ad libitum-fed or 16 h fasted group. n = 6–9 mice per group. (D) Hepatic lipid secretion analysis with HFD-fed flox and LTKO mice. n = 6 mice for flox and 9 mice for LTKO. (E, F) De novo lipogenesis activity in livers from HFD-fed flox and LTKO mice. n = 8 mice for flox and n = 4 mice for LTKO. N.S., no significance (Student t-test). (G) Fatty acid uptake in primary hepatocytes from NCD-fed flox or LTKO mice. n = 8 replicates per group. (H, I) Serum levels of β-hydroxybutyrate (BOH) (H) and total ketone bodies (TKB) (I) in HFD-fed flox or LTKO mice upon 16 h fasting. n = 5–6 mice per group. *p < 0.05 (Student t-test). (J) 14C-palmitate oxidation activity in primary hepatocytes from flox or LTKO mice. n = 6 replicates per group. ***p < 0.001 (Student t-test). (K) Complete oxidation rate by 14C-palmitate. n = 6 replicates per group. **p < 0.01 (Student t test). For the data in (A), (B), (C), (D), and (G), *p < 0.05 for flox compared to LTKO in same feeding condition, #p < 0.05, ##p < 0.01 for fed compared to fasting in each genotype, N.S.; no significance between genotypes; p > 0.05 (two-way ANOVA followed Holm-Sidak’s multiple comparisons test). All data in the figure are shown as the mean ± SEM. See also Figure S4.