Insulin Detemir is a long-acting synthetic insulin analogue that effectively controls blood glucose levels by stimulating GLP-1 secretion through enhanced glucagon gene expression and activation of Akt- and/or ERK-dependent signaling pathways. Insulin Detemir is widely employed in type 2 diabetes research to investigate molecular mechanisms of insulin signaling, glucose homeostasis, and therapeutic interventions.

For primary fetal rat intestinal cell (FRIC) cultures, Insulin Detemir (100 nM, 0.5-4 hours) can upregulate the expression level of Gcg mRNA, while Insulin Detemir (100 nM, 5 minutes and 10 minutes) induces rapid phosphorylation of Akt [1].
When Insulin Detemir (100 nM) acts for 5-120 minutes, it not only increases the phosphorylation level of β-catenin and promotes its nuclear translocation, but also enhances the phosphorylation of cAMP response element-binding protein (CREB) in a manner dependent on phosphatidylinositol 3-kinase and/or mitogen-activated protein kinase kinase/extracellular signal-regulated kinase [1].

When Insulin Detemir is administered via intraperitoneal injection at a dose of 5 IU/kg, once daily for 2 weeks, it not only reduces body weight compared to other insulin preparations but also exhibits a preferential effect on intestinal tissues. This phenomenon may be associated with the activation of the insulin/catenin/CREB signaling pathway [1].