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Upadacitinib as induction and maintenance therapy for moderately to severely active ulcerative colitis: results from three phase 3, multicentre, double-blind, randomised trials

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Thus, postprandial PYY release under normal physiological conditions is likely to be mediated through paracrine and neural mechanisms (123)

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Given the established clinical use of GLP-1RAs for the treatment of T2DM, preclinical and clinical research was centered largely around DR, which suggested the neuropathologic protective effects of GLP-1 are due to downregulation of NF-B, proinflammatory cytokines such as TNF-alpha and IL-1beta, and VEGF

The glucagon receptor activation unique to retatrutide likely drives this effect, though the exact mechanism remains under investigation