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Our and this finding imply that enhanced activation of afferent renal nerves by GLP-1 in HF is dependent on the expression levels of GLP-1R rather than the concentrations of GLP-1 itself in the renal pelvis

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I reassure patients that it's something that we can improve, so there's no need to stop a medication that is otherwise working well

The additional GIP receptor engagement is thought to amplify satiety signaling in the hypothalamus and augment insulin secretion in a glucose-dependent fashion, without proportionally increasing nausea at therapeutic doses

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Cell Death Dis 8 , e2848 (2017)