Insulin Detemir

Insulin Detemir is an artificial insulin, shows effect on controlling blood sugar levels. Insulin Detemir stimulates GLP-1 secretion as a consequence of enhanced Gcg expression by a mechanism involving activation of Akt- and/or extracellular signal-regulated kinase (ERK)-dependent-cat and CREB signaling pathways. Insulin Detemir can be used for type 2 diabetes research[1][2].

Signaling Pathways >> PI3K/Akt/mTOR >> Akt

Research Areas >> Metabolic Disease

Signaling Pathways >> MAPK/ERK Pathway >> ERK

Signaling Pathways >> Stem Cell/Wnt >> ERK

Insulin Detemir (d-INS) (100 nM; 0.5-4 h) increases Gcg mRNA expression in primary fetal rat intestinal cell (FRIC) cultures, and (100 nM; 5 min and 10 min) induces rapid phosphorylation of Akt, as well[1]. Insulin Detemir (100 nM; 5-120 min) increases β-catenin phosphorylation, its nuclear translocation, and enhances cAMP response element-binding protein (CREB) phosphorylation in a phosphatidylinositol 3-kinase and/or mitogen-activated protein kinase kinase/extracellular signal-regulated kinase-sensitive manner[1]. Western Blot Analysis[1] Cell Line: GLUTag cells Concentration: 100 nM Incubation Time: 0, 5, 10, 30, 60, and 120 min Result: Stimulated CREB, ERK1/2, Akt and its downstream glycogen synthase kinase (GSK)-3 phosphorylation at 5 min and 10 min.

Insulin Detemir (d-INS) (5 IU/kg; i.p.; once daily; 2 weeks) demonstrates weight-sparing effects compared with other insulin formulations, and shows a intestinal tissues preference, potentially involving the activation of insulin/-catenin/CREB signaling pathways[1]. Animal Model: Obese type 2 diabetic db/db mice[1] Dosage: 5 IU/kg Administration: Intraperitoneal injection; once daily for 2 weeks Result: Decreased body weight of the mice after 14-day daily injection of d-INS (5 IU/kg) significantly compared with those injected with the same dose of human Insulin or saline. Induced rapid phosphorylation of protein kinase B (Akt) in the gut L cells of normal mice.

[1]. Liu S, et al. Insulin detemir enhances proglucagon gene expression in the intestinal L cells via stimulating β-catenin and CREB activities. Am J Physiol Endocrinol Metab. 2012 Sep 15;303(6):E740-51.