Short answer first, then the reasoning. Most of what circulates confidently in this community traces back to one summary of one study, and the qualifier was dropped somewhere in the third retelling.

kate.chem said:

Most of what circulates confidently in this community traces back to one summary of one study, and the qualifier was dropped somewhere in the third…

Agreeing with kate.chem, and the qualification matters more than the agreement. 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.

Happy to go further on any of that.

newstart_MO said:

Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.

This is my experience too, for whatever a second data point is worth. Posting only so the count is not one.

Adding the clinical framing, because it changes how the question reads. The useful move here is to separate what is established from what is widely repeated. Those two sets overlap less than the confident tone of most write-ups suggests, and the second set is where nearly all the disagreement on this board comes from.

That is the short version; the long version is somebody else's post.