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The nature of this compensatory mechanism in GLP-1 receptor KO mice at high oral glucose load is not known but deserves further studies candidates may be the higher baseline glucose levels or compensatory increase in other gut hormones which may mask the consequence of GLP-1 receptor gene deletion

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The lack of commonly available and sufficiently selective antibodies to detect GIPR further remains a notable limitation that hinders in-depth immunohistochemical analysis of GIPR in the brain