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Among patients with PMOS and related metabolic conditions such as obesity, these therapies may be prescribed for labeled metabolic indications while still shaping the broader PMOS care pathway

The results indicate that Gipr -expressing cells in the AP underlie the ability of GIPR agonists to reduce food intake in lean and DIO mice and, taken together with the previous report that GABAergic Gipr KO mice do not exhibit reduced food intake in response to acyl-GIP, suggest that subpopulations of GABAergic Gipr -expressing neurones located in the AP mediate both the appetite-suppressing and anti-aversive effects of exogenous GIPR agonists 6

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