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.
The question I want answered is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
Taking the question as asked, rather than the general version of it. The honest answer is that the effect is real, the magnitude is contested, and the individual variation is larger than either. Those three things can all be true at once, and most arguments here are two people holding different parts of that.
SarahChen_PharmD said:The honest answer is that the effect is real, the magnitude is contested, and the individual variation is larger than either.
Agreeing with SarahChen_PharmD, 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.
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Browse GL Biochemanna.melb_AU 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.
From the other side of the consultation, briefly. It helps to ask what evidence would change your mind before you look at any. If nothing would, the discussion is not about evidence, and it is better to say so early than to spend nine posts discovering it.