Dr.CardioMD said:

Albumin binding above 99% is the whole reason weekly dosing works, and it is also why the trough matters more than the peak.

This is where I part company with the consensus forming above. The trial means are being read too generously in this thread. STEP populations were selected, supported, and titrated by protocol, and the real-world curves are consistently a few points worse. That difference is not noise, it is what happens when you remove the study infrastructure.

One concrete data point for the thread. Worth knowing that the injection site changes very little. Abdomen, thigh and upper arm are bioequivalent for semaglutide, so a site change is not a plausible explanation for a bad week.

Worth separating that from liver and MASH, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.

JessicaH_TX said:

The trial means are being read too generously in this thread.

Adding the part of the answer the thread has not reached. 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.

A 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?

OP back with an update, since a thread like this is useless without one.

Following this thread I went back and re-read the extension data properly. The point about trough rather than peak explains the pattern I was seeing on day six, which I had been blaming on the vial.