Collecting this in one place because it comes up every few weeks and the answer is always assembled from scratch. It is about liver and MASH, and it is deliberately narrow — everything I am not confident about is marked as such.
What is actually established
The liver data is among the strongest non-weight findings in the class. The semaglutide MASH programme reported a large advantage over placebo on MASH resolution, with a substantial minority also achieving fibrosis improvement — and fibrosis is the endpoint that predicts outcomes. Mechanistically it is reduced hepatic lipogenesis, increased fatty-acid oxidation, less hepatic inflammation, and possibly a direct effect on stellate-cell activation.
The condition it depends on
ALT falling is not the same as fibrosis improving. Enzymes are a crude proxy; FIB-4 or elastography is what tells you about the thing that matters.
The practical version
With resmetirom now available for MASH, combination approaches are being explored, so the standard of care in this area is moving faster than most threads assume.
What I am not sure about
What I am after is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is. I have searched first, so if this is covered somewhere point me at it and I will read it.
cory_ATX said:The liver data is among the strongest non-weight findings in the class.
Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
Baseline: "Moderate hepatic steatosis, liver span 17.2cm, echogenic texture consistent with fat infiltration"
Month 8: "Mild steatosis, liver span 15.8cm, improved echogenicity"
Month 14: "Minimal to no steatosis, normal liver span 14.5cm, normal echotexture"
My liver literally shrank and de-fattened. The ultrasound tech said she's seen this pattern increasingly in GLP-1 patients and it's remarkable how consistently the fatty liver resolves.
cory_ATX said:The liver data is among the strongest non-weight findings in the class.
Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD). After 9 months on GLP-1 therapy:
| Marker | Baseline | Current | Normal Range |
|---|---|---|---|
| ALT | 66 | 23 | 7-56 U/L |
| AST | 59 | 23 | 10-40 U/L |
| GGT | 86 | 31 | 9-48 U/L |
| ALP | 106 | 78 | 44-147 U/L |
FibroScan also improved — liver stiffness from 8.5 kPa to 6.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.
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View ResultsTirzTom said:Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD).
Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 312 dB/m (moderate steatosis) and stiffness 8.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 10 months: CAP dropped to 235 dB/m (minimal steatosis) and stiffness normalized to 4.8 kPa. Hepatologist says the liver is essentially healing itself as the metabolic stress resolves.
GLP-1 agonists may become first-line NASH therapy. The Phase 3 data on semaglutide for NASH is very promising.
Dr.GutHealth said:Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
Mine went the same way, slower.