Non-invasive MASH biomarkers — my results so far

Dr.GutHealth said:

Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD).

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.

nick_newbie 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.

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.

VendorMark said:

NASH/MAFLD therapeutic landscape and liver and MASH: GLP-1 agonists are emerging as potential first-line NASH therapy.

Adding the part of the answer the thread has not reached. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.

Following on from mel_PDX — and this may be the naive question:

Did your prescriber agree with that reading, and if not what was their objection?

Reporting back.

Coming back a few months on. It held. Nothing dramatic to report, which is the report.