Bioexplorer
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So it seems like the impact on perceived inflammation reduction of sema, tirz, and reta depends on the right balance of GLP-1 and GIP agonist effects. But it gets puzzling when you consider that tirz is better at reducing inflammation than sema with no GIP effect and reta is a stronger GIP agonist than tirz but apparently not as effective at perceived inflammation reduction.
Does the glucagon agonist effect of reta counter some of the benefits of the GIP and GLP-1 components of the peptide? Or is there some unknown non incretin mimetic effect of tirz?
Does the glucagon agonist effect of reta counter some of the benefits of the GIP and GLP-1 components of the peptide? Or is there some unknown non incretin mimetic effect of tirz?