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Cell culture studies demonstrate that GLP3 exhibits differential potency across its three target receptors: it is approximately 8.9-fold more potent at the human GIP receptor (EC50: 0.0643 nM) compared to the endogenous GIP ligand, while showing reduced potency at GLP-1 receptors (0.4-fold, EC50: 0.775 nM) and glucagon receptors (0.3-fold, EC50: 5.79 nM) relative to their native hormones[3]

In turn, HIF1 regulates GLUT1 expression and, together with TRIB3, increases the influx of glucose in the retina, 109 aggravating metabolism disorder