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Its mechanism involves specific engagement of AMY1R and AMY3R in hindbrain and hypothalamic circuits that regulate energy homeostasis, leading to preferential fat mass reduction and altered hypothalamic gene expression profiles [2]
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Die zustzliche Glukagon-Rezeptor-Aktivierung unterscheidet Retatrutide von dualen GIP/GLP-1-Agonisten und resultiert in einer hepatischen cAMP-Signaltransduktion, die in Tiermodellen mit einer Steigerung des Energieumsatzes und der hepatischen Lipidoxidation korrelierte
The molecular basis for the prolonged blood circulation of lipidated incretin peptides :peptide oligomerization or binding to serum albumin
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