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This results in a lower ability to promote receptor internalization compared with endogenous GLP-1, so it allows to have an increased GLP-1R expression on the cell surface, which translates in more robust insulinotropic properties, possibly explaining the enhanced insulin secretion (in both diabetic and not diabetic human islets), induced by TZP (19) by approximately 25% more than the one induced by only one of the two agents

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