Subsequent studies have shown that low physiological concentrations of GLP-1 are indeed ineffective in patients with T2DM (76), whereas larger slightly supraphysiological doses [like those employed by Nauck et al. (74)] could in fact normalize beta cell sensitivity to glucose (77); in contrast, GIP remains inactive in T2DM regardless of dose (77). Here, GLP1R is linked to type 2 diabetes mellitus.