Fatty liver on an incidental scan two years ago and nobody followed it up. Now that I am losing weight I would like to know what to re-measure.
What would genuinely help is knowing whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is.
Tell me what I have not thought of.
nick_newbie said:Fatty liver on an incidental scan two years ago and nobody followed it up.
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.
PeptideChemSF said: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…
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 | 66 | 28 | 7-56 U/L |
| AST | 54 | 26 | 10-40 U/L |
| GGT | 91 | 30 | 9-48 U/L |
| ALP | 101 | 83 | 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 Standardsnick_newbie said:Fatty liver on an incidental scan two years ago and nobody followed it up.
This matches mine closely enough to be worth saying so out loud. Posting only so the count is not one.
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.