Bioexplorer
Explorer
So the degree to which sema, tirz, and reta appear to lower inflammation seems tied to getting the GLP-1 and GIP agonist mix just right. Yet it gets confusing: tirz does a better job at reducing inflammation than sema, which has no GIP effect, while reta is a stronger GIP agonist than tirz but apparently does not reduce perceived inflammation as well.
Could reta's glucagon agonist action be blunting some of the upside from its GIP and GLP-1 parts? Or does tirz have some non-incretin mimetic effect that we don't yet know about?
Could reta's glucagon agonist action be blunting some of the upside from its GIP and GLP-1 parts? Or does tirz have some non-incretin mimetic effect that we don't yet know about?