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.
Numbers rather than impressions, if you have them.
Taking the question as asked, rather than the general version of it. Take it one variable at a time. Almost every unanswerable question in these threads is unanswerable because three things changed in the same fortnight, and no amount of subsequent argument can untangle them after the fact.
If somebody has the primary source to hand I would rather cite it than paraphrase it.
CarlaRPh_TPA said:Almost every unanswerable question in these threads is unanswerable because three things changed in the same fortnight, and no amount of subsequent…
Agreeing with CarlaRPh_TPA, 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 Biochemandrew_nyc 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.
Mine went the same way, slower. Posting only so the count is not one.
From the other side of the consultation, briefly. 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.