FIGURE

Figure 1

ID

ZDB-FIG-231002-325

Publication

Zhou et al., 2023 - Inhibition of mitochondrial fatty acid β-oxidation activates mTORC1 pathway and protein synthesis via Gcn5-dependent acetylation of raptor in zebrafish

Other Figures

All Figure Page

Back to All Figure Page

Figure 1

Mitochondrial FAO inhibition activates the mTORC1 pathway and increases protein synthesis in zebrafish.A, isotope tracer analysis (PA∗, [1–14C] palmitic acid) to assess mitochondrial FAO efficiency in liver and muscle tissues. N = 6. B–E, the effects of mitochondrial FAO inhibition by mildronate (MD) on muscle protein content (B, n = 5), carcass protein content (C, n = 5), whole body protein content (D, n = 5), and carcass ratio (CR) (E, n = 9) in zebrafish. CR = 100 × (carcass weight/body weight). The carcass is mainly muscle tissue. F and G, the mTORC1 activity in liver (F) and muscle (G) tissues was detected by Western blotting for key proteins of the mTORC1 pathway. p indicates phosphorylated protein. Liver and muscle tissues were lysed, and Western blots for p-mTOR^Ser2448, p-S6k^Thr389, S6k, p-S6^Ser235/236, and S6 are shown. N = 3. H, metabolic tracking of [1–14C]-PA and l-[14C (U)]-AA in zebrafish-fed CN and MD diets for 6 weeks (H). N = 6. Data represent mean ± SD. ∗p < 0.05 and ∗∗p < 0.01. AA, amino acid; CN, control; FAO, fatty acid oxidation; mTORC1, mechanistic target of rapamycin complex 1.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ J. Biol. Chem.