Taking the question as asked, rather than the general version of it. There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.

NurseKim_ATL said:

There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.

NurseKim_ATL has the substance of this right. The condition it depends on is worth stating. 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.

BethLabQueen 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. The detail I would add is minor and it is already implied above.

Clinical perspective, offered as context rather than as advice. If two explanations both fit, the useful question is which one predicts something the other does not. That is answerable; arguing about which sounds more plausible is not.