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In contrast to the results of our previous experiments performed using pancreatic islets (i.e., those in which GEP44-mediated effects were more prominent in the presence of the Y1-R antagonist), we found that GEP44 directly increased glucose uptake in muscle tissue to a similar degree to that elicited by PYY 1-36 and that GEP44-mediated glucose uptake was inhibited by Y1-R antagonism

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Since they activate the same receptor (GHSR-1a), combining them wouldn't produce the same synergy as pairing either with a GHRH analog (which uses a different receptor)