JennaRN said:

Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.

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.

laura_annarbor 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.

PharmD_Rodriguez said:

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

Coming at PharmD_Rodriguez’s question from a different direction. It helps to ask what evidence would change your mind before you look at any. If nothing would, the discussion is not about evidence, and it is better to say so early than to spend nine posts discovering it.

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

How would you tell the difference between that and the alternative explanation?

Reporting back.

Update: the thing I was blaming turned out not to be the cause. Leaving the original post as written rather than editing it, so the mistake stays visible for whoever searches this next.