TinaHashiRN said:No disagreement, though it depends on where somebody is starting from, and this thread has been assuming a starting point nobody stated.
Same pattern here, and in the same order. The detail I would add is minor and it is already implied above.
TinaHashiRN said:No disagreement, though it depends on where somebody is starting from, and this thread has been assuming a starting point nobody stated.
There is a second half to this that has not been said yet. 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.
Ask again with the specifics and you will get a better answer than this one.
One concrete data point for the thread. For anyone reading later: the numbers in this thread are worth checking against a primary source before you act on them, including mine. Half the figures circulating in this community trace back to a secondary summary that dropped a qualifier.
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Browse GL BiochemA narrower follow-up, since the general answer is now clear:
Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?
PeptideSynthNJ said:For anyone reading later: the numbers in this thread are worth checking against a primary source before you act on them, including mine.
I read this differently from PeptideSynthNJ, on substance rather than tone. The counter-case has not been addressed. Somebody upthread described the situation that does not fit, and the thread moved on rather than engaging with it, which is the failure mode this board is supposed to avoid.