Posting this because the summary going around does not say what the paper says, and the difference matters for how people here are using it.
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.
Where I think it is weakest: the comparator does most of the work in how this gets reported, and it is not the comparator most people think they are citing.
The bit I cannot resolve on my own is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is. Not looking for reassurance. Looking for the part I have got wrong.
Figures above are from the primary publication rather than the press summary. If a number here disagrees with one you have, post yours and we will work out which of us is reading a secondary source.
Dr.KarenChen 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.
Dr.KarenChen said:The liver data is among the strongest non-weight findings in the class.
Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 325 dB/m (moderate steatosis) and stiffness 9.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 11 months: CAP dropped to 228 dB/m (minimal steatosis) and stiffness normalized to 6.1 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.
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Shop Reference StandardsPeptideChemSF said:Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 325 dB/m (moderate steatosis) and stiffness 9.8 kPa (possible…
Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD). After 11 months on GLP-1 therapy:
| Marker | Baseline | Current | Normal Range |
|---|---|---|---|
| ALT | 62 | 29 | 7-56 U/L |
| AST | 65 | 25 | 10-40 U/L |
| GGT | 82 | 33 | 9-48 U/L |
| ALP | 112 | 74 | 44-147 U/L |
FibroScan also improved — liver stiffness from 10.5 kPa to 6.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.
BariatricNurseD said:Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
This is my experience too, for whatever a second data point is worth.