Fig. 6: Hepatic cysteine availability is a key determinant of hepatic CoA synthesis and maximal fatty acid oxidation capacity. | Nature Communications

Fig. 6: Hepatic cysteine availability is a key determinant of hepatic CoA synthesis and maximal fatty acid oxidation capacity.

From: TFEB regulates sulfur amino acid and coenzyme A metabolism to support hepatic metabolic adaptation and redox homeostasis

Fig. 6

a–i Male 10 weeks old C57BL/6 J mice were fed isocaloric Western diet containing 20% protein, 5% protein or 5% protein with added cystine (Cys) for 6 weeks. Mice were euthanized after 6 h fast. Liver tissues were used for metabolomics analysis (n = 4). Relative abundance of liver metabolites is shown with control arbitrarily set as 1. All results are mean ± SEM. A p value < 0.05 is considered statistically significant (One-way ANOVA and post hoc Dunnett test). GSH reduced glutathione, SAMs S-adenosylmethionine, SAH S-adenosylhomocysteine, CoA coenzyme A. j. AML12 cells were cultured in medium containing 200 μM (High) or 20 μM (Low) methionine and cystine overnight. Seahorse XF palmitate oxidation stress test was performed in live cells under basal and FCCP-induced mitochondrial uncoupled conditions as described in Methods. Results are expressed as mean ± SD (technical repeats). The results are from one of two independent experiments. Unpaired 2-tailed t-test was used to calculate the p values. BSA bovine serum albumin, PA palmitate (complexed to BSA). k. AML12 cells were cultured in medium containing 200 μM (High) or 20 μM (Low) methionine and cystine overnight. Lipid droplets were visualized with BODIPY staining and nuclei were visualized with DAPI staining. Representative fluorescence images from 3 independent experiments are shown. Scale bar: 125 μm. Source data for (a–j) are provided as a Source Data file.

Back to article page