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.
For anyone tracking the class: GLP-1 alone gets you appetite, GLP-1 plus GIP adds tolerability and lipid handling, and adding glucagon adds expenditure and liver-fat reduction. Each addition also adds a receptor system that can generate side effects.
What I am trying to establish is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Practical detail welcome, however dull — the duller the better.
This one has a reasonably settled answer, so here it is. 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.
COA_Karl said:It helps to say which part of this you are uncertain about.
That is correct as far as it goes, and here is where it stops going. 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 Biochemamsterdam_pete 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. I had assumed I was the exception until I read this.
From the other side of the consultation, briefly. 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.