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Glp1r / mice, and, to a greater extent, Glp1r / : Gipr / mice, exhibit defective glucose-stimulated insulin secretion, subnormal upregulation of insulin gene expression in response to high-fat diet (HFD) feeding, and impaired glucose tolerance (3, 4)
The primary objective of this study is to examine the dose-response relationship of semaglutide and glycemic control in order to determine an optimal dose and administration regiment
