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All hormone and substrate profiles except non-esterified fatty acids (NEFA) and cholecystokinin (CCK) were significantly suppressed (GLP-2 completely suppressed) during the GLP-1 infusion, whereas profiles of NEFA and CCK differed in time course during the two treatments (treatmenttime effect), P<0.0001)

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Conclusion A population pharmacokinetic model incorporating allometric scaling was developed to simultaneously describe the PK of semaglutide in all animal species and predict its PK in humans