Source comparison
MOTS-c Visceral Fat Reduction Research Mechanism: Treatment Comparison
MOTS-c (15mg daily) AMPK activation in visceral adipocytes; mitochondrial-derived peptide increases fat oxidation and glucose uptake 4.1% reduction in VAT mass (DEXA-measured) No statistically significant change 18–22% improvement in HOMA-IR score Targets meta
This comparison does not assign a generated winner or score.
- MOTS-c (15mg daily)
- AMPK activation in visceral adipocytes; mitochondrial-derived peptide increases fat oxidation and glucose uptake
- 4.1% reduction in VAT mass (DEXA-measured)
- No statistically significant change
- 18–22% improvement in HOMA-IR score
- Targets metabolically harmful fat without proportional subcutaneous loss; mechanism-specific but human data still limited
- GLP-1 Agonist (semaglutide 2.4mg weekly)
- Appetite suppression via hypothalamic GLP-1 receptor activation; delays gastric emptying
- 8–12% total body weight loss (VAT reduces proportionally)
- Significant reduction (proportional to total weight loss)
- 25–35% improvement in insulin sensitivity
- Proven efficacy for total weight loss; VAT reduction is secondary to overall fat loss, not selective
- Caloric Restriction (500 kcal/day deficit)
- Energy imbalance forces lipolysis; no tissue selectivity
- Variable; approximately 5–7% VAT reduction with 5% total weight loss
- Proportional reduction
- 10–15% improvement if weight loss sustained
- Effective but requires sustained adherence; no selectivity. Loses subcutaneous and visceral fat equally
- Metformin (2000mg daily)
- AMPK activation in liver and muscle; reduces hepatic glucose output
- Minimal direct effect on VAT mass (<2% over 12 weeks)
- Minimal
- 8–12% improvement in insulin sensitivity
- Improves glucose control but not a fat loss agent; AMPK activation occurs but doesn't translate to significant lipolysis