Taking the question as asked, rather than the general version of it. The glucagon component looks paradoxical and is not. Glucagon receptor agonism raises energy expenditure and drives hepatic fatty-acid oxidation, and its hyperglycaemic tendency is offset by the GLP-1 arm's insulin secretagogue effect. Net result: intake down from GLP-1/GIP, expenditure up from glucagon, glycaemia neutral or improved. It is a balancing act, and it is why the liver-fat results are the most interesting part of the dataset.

TrialNerd_Beth said:

The glucagon component looks paradoxical and is not.

Fair, but phase 2 tolerability figures rarely survive contact with phase 3 scale. Triple agonism means three receptor systems generating adverse events, and the dropout column is the one I would read first when the larger trials report.

labquiet_amy said:

Triglycerides dropped by half, HDL barely moved, and my calculated LDL is almost exactly where it started, which is not the outcome I had been…

Adding a me-too, because a thread of one person's experience is not much use.

From the other side of the consultation, briefly.

Comprehensive lipid panel update relevant to the lipid panel:

The triglyceride drop is the most impressive. My cardiologist reduced my statin dose based on these results.