Understand the source comparison
Peptides Help Fatty Liver vs GLP-1 Drugs: Mechanism Comparison
AOD-9604 AMPK activation → inhibits ACC → reduced hepatic lipogenesis 31% reduction in 12 weeks (Phase 2 RCT, n=42) No—effect localised to hepatic tissue Phase 2 complete, no Phase 3 trials initiated Most direct hepatic mechanism with no systemic metabolic sid
No winner is assigned.
This page preserves a source comparison for education. It does not add a rating, recommendation or clinical judgment.
- AOD-9604
- AMPK activation → inhibits ACC → reduced hepatic lipogenesis
- 31% reduction in 12 weeks (Phase 2 RCT, n=42)
- No—effect localised to hepatic tissue
- Phase 2 complete, no Phase 3 trials initiated
- Most direct hepatic mechanism with no systemic metabolic side effects, but lacks large-scale validation
- MOTS-c
- Enhances mitochondrial respiration → improves insulin sensitivity → reduces SREBP-1c activation
- 38–42% reduction in preclinical models
- Minimal—insulin sensitisation occurs independently of weight loss
- Preclinical only, human trials in progress
- Strongest mitochondrial rationale, but zero published human data for NAFLD as of 2026
- GLP-1 Agonists (semaglutide, liraglutide)
- Weight loss reduces FFA supply + direct GLP-1R activation in hepatocytes reduces inflammation
- 33–39% reduction in 12–68 weeks (multiple Phase 3 RCTs)
- Partially—direct hepatic effect exists but enhanced by weight loss
- FDA-approved for diabetes/obesity, off-label use common for NAFLD
- Most evidence, most accessible, but side effect profile (nausea, vomiting) limits adherence in 30% of patients
- Thymalin
- Immune modulation → reduces hepatic inflammation (theoretical)
- No published clinical data for NAFLD
- Unknown
- No trials for fatty liver specifically
- Thymalin shows immunomodulatory effects in other contexts, but hepatic fat reduction mechanism unproven