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autore: Antonino Tornatore Copyright 2005 - 2026
173 the GIPR has not until recently been intensively pursued as a T2D treat ment target, primarily due to GIP responses being blunted in T2D patients (6) and the
174 perception that GIPR activation leads to weight gain, as inferred from the
175 observation that GIPR knockout (KO) mice are protected
176 against the effects of an obesogenic diet (7).
177 As a result, antagonizing rather than activating the GIPR has been suggested as a potential therapeutic intervention for diabetes and obesity (8, 9).
178 However, recent data from preclinical and clinical studies ap pear to contradict these
179 assumptions regarding the role of GIPR in diabetes, as GIPR agonists have been shown to
180 im prove glucose tolerance and reduce body weight in T2D pa tients (10), and dual GLP-1R/GIPR
