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In 1990 Mojsov and colleagues also described the existence of a second biologically active form of GLP-1, labelled GLP-1 (7-36) amide, in the intestines (Mojsov, Kopczynski, Habener)

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The gastrointestinal effects result primarily from delayed gastric emptying and altered gut motility

The GIP receptor displays higher basal activity than the GLP-1 receptor but does not recruit GRK2 or arrestin3 effectively

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This phenomenon may be the result of its unbalanced dual agonistic effect, favoring GIPR over GLP-1R activity [7], because dose escalation of selective GLP-1R agonists induces undesirable gastrointestinal effects