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Along with preclinical data indicating that long-acting GIPR agonists act in the brain to decrease body weight and food intake via GIPR signalling in inhibitory -aminobutyric acid-producing (GABAergic) neurons 5,6,7 , and by mitigating the emetic effects of GLP-1R agonism 8,9 , GIPRGLP-1R co-agonism has been established as a highly effective strategy for the management of obesity, type 2 diabetes and MASH

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They act by inhibiting the NF-kB activation pathways [68, 69]

two in the control group, without any significant difference between the groups (6.8% vs