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 narrow version of the question is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
I would rather have one careful answer than five confident ones.
This one has a reasonably settled answer, so here it is. 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.
Dr.NutriCornell said:It helps to ask what evidence would change your mind before you look at any.
Dr.NutriCornell 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.
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Browse GL Biochemraj_cambridge 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. Nothing to add that would improve it.
Clinical perspective, offered as context rather than as advice. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.
Ask again with the specifics and you will get a better answer than this one.