ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.
What would genuinely help is knowing 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.
MASHdoc_SA said:ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.
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 | 76 | 23 | 7-56 U/L |
| AST | 49 | 25 | 10-40 U/L |
| GGT | 86 | 37 | 9-48 U/L |
| ALP | 96 | 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.
Dr.ObesityLA said:Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD).
ATTAIN trial (survodutide) context for liver and MASH: survodutide, a GLP-1/glucagon dual agonist, showed -18.7% body weight at 46 weeks in the Phase 3 ATTAIN trial. NASH resolution was achieved in ~60% of patients[1].
This is relevant to liver and MASH because survodutide's glucagon agonism specifically targets hepatic lipid metabolism — making it potentially the best-in-class agent for NASH/MAFLD comorbid with obesity.
[1] Sanyal AJ, et al. N Engl J Med. 2024.
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View ResultsMASHdoc_SA said:ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.
This is my experience too, for whatever a second data point is worth. I had assumed I was the exception until I read this.
Adding the clinical framing, because it changes how the question reads.
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.