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 bit I cannot resolve on my own is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Tell me what I have not thought of.
Taking the question as asked, rather than the general version of it. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.
SarahChen_PharmD said:The mechanism and the magnitude are separate questions.
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 Biochemdenise_HTX 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.
Same pattern here, and in the same order. The detail I would add is minor and it is already implied above.
Clinical perspective, offered as context rather than as advice. It helps to say which part of this you are uncertain about. A precise question gets a precise answer; a general one gets everybody’s favourite anecdote.