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Together these data suggest that increased postprandial serotonin may contribute to the pathophysiology of PBH and provide a potential therapeutic target

The conventional concern that glucagon raises blood glucose and would offset the glucose-lowering goal of GLP-1/GIP agonism is addressed in the published mechanism literature by examining the tissue-specific and timing-specific actions of each receptor arm

In most cases, there is no reason to discontinue GLP-1 treatment unless another specific medical indication arises

It's also possible that GLP- 1 affects cells indirectly

This triple mechanism explains why clinical trials showed weight loss results exceeding all previous medications in this class

Nature 541 (7638), 481487