Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Pathway analysis of livers from mice with NASH.
  • Fig. S2. Correlation between gene expression and hepatic fat in humans.
  • Fig. S3. Agxt1+/+ and Agxt1−/− mice are comparable on CD.
  • Fig. S4. NAFLD-related parameters in Agxt1+/+ and Agxt1−/− mice fed NASH diet.
  • Fig. S5. Glycine deficiency exacerbates WD-induced obesity.
  • Fig. S6. Glycine deficiency exacerbates WD-induced hyperlipidemia and HS.
  • Fig. S7. Glycine-based compounds.
  • Fig. S8. Effects of glycine-based compounds on glucose tolerance.
  • Fig. S9. Lipid-lowering effects of DT-109.
  • Fig. S10. Glycine or DT-109 prevent WD-induced HS.
  • Fig. S11. Confirmation of NASH before randomization to experimental groups.
  • Fig. S12. Metabolic effects of DT-109 in mice with established NASH.
  • Fig. S13. DT-109 protects against diet-induced NASH.
  • Fig. S14. Major shifts in the gut microbiome of mice with NASH.
  • Fig. S15. Clostridium sensu stricto is overrepresented in mice with NASH.
  • Fig. S16. Gut microbiome alterations after 2 weeks of treatments while on NASH diet.
  • Fig. S17. Gut microbiome alterations after 10 weeks of treatments while on NASH diet.
  • Fig. S18. Gut microbiome alterations during DT-109 treatment while on CD.
  • Fig. S19. DT-109 reverses NASH diet–induced liver transcriptome alterations.
  • Fig. S20. Pathway analysis of livers from mice on CD versus NASH diet.
  • Fig. S21. Pathway analysis of livers from mice on NASH and treated with H2O versus DT-109.
  • Table S1. Previous clinical evidences associating lower circulating glycine with NAFLD and other cardiometabolic diseases.
  • Table S2. Composition of the amino acid–defined WD with or without glycine (WDAA +/− Gly).
  • Table S3. Primers used for qPCR analyses.
  • References (6175)

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