Read the primary source rather than the write-up and the two do not agree, so here is what is actually in 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 population was selected and supported in ways a real cohort is not, so I would read the effect size as a ceiling rather than an expectation.
What I am after is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is. Happy to be told the question itself is 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.
tane_welly said:The liver data is among the strongest non-weight findings in the class.
NASH/MAFLD therapeutic landscape and liver and MASH: GLP-1 agonists are emerging as potential first-line NASH therapy. The Phase 2b data for semaglutide showed 59% NASH resolution (vs 17% placebo) with 43% achieving fibrosis improvement[1].
Mechanism: GLP-1R activation reduces hepatic lipogenesis, increases fatty acid oxidation, reduces hepatic inflammation, and may directly reduce hepatic stellate cell activation (fibrosis pathway).
With resmetirom (thyroid hormone receptor agonist) recently approved for NASH, the field is evolving rapidly. Combination approaches (GLP-1 + resmetirom) are being explored.
[1] Newsome PN, et al. N Engl J Med. 2021;384(12):1113-1124.
tane_welly 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 8 months on GLP-1 therapy:
| Marker | Baseline | Current | Normal Range |
|---|---|---|---|
| ALT | 70 | 22 | 7-56 U/L |
| AST | 48 | 24 | 10-40 U/L |
| GGT | 85 | 36 | 9-48 U/L |
| ALP | 95 | 77 | 44-147 U/L |
FibroScan also improved — liver stiffness from 10.5 kPa to 5.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.
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Shop Reference StandardsDr.CardioMD 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 324 dB/m (moderate steatosis) and stiffness 8.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 10 months: CAP dropped to 237 dB/m (minimal steatosis) and stiffness normalized to 6 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.
LipidDoc_ATL said:NASH/MAFLD therapeutic landscape and liver and MASH: GLP-1 agonists are emerging as potential first-line NASH therapy.
This is my experience too, for whatever a second data point is worth. Nothing to add that would improve it.