GLP-1(28-36)amide acetate 抑制线粒体通透性转变，具有抗氧化、抗糖尿病和心脏保护活性。

GLP-1(28-36)amide acetate inhibits mitochondrial permeability transition with antioxidant, anti-diabetic and cardioprotection activities.

The plasma half-life of GLP-1(28-36)amide acetate is longer in human hepatocytes (24 min) than that in mouse hepatocytes (13 min). GLP-1(28-36)amide acetate (100 nM) on hepatocytes modulates mitochondrial oxidative metabolism including gluconeogenesis in mitochondria of hepatocytes[1].

In high-fat diet-fed mice, GLP-1(28-36)amide acetate (18.5 nmol/kg) improved hepatic glucose disposal. In diet-induced obese mice, GLP-1(28-36)amide acetate (18.5 nmol/kg BW/day) diminishes the development of hepatic steatosis. In male C57BL6/J mice, administration of GLP-1(28-36)amide acetate for 20 min to, then isolated hearts underwent 30 min of global ischemia and 40 min of reperfusion, the recovery of left ventricular developed pressure is significantly great. In a β-cell injury diabetic mouse model, GLP-1(28-36)amide acetate (18 nmol/kg; i.p.) shows cytoprotective effect on pancreatic β cells by promoting proliferation and increasing mass[1].

T37890L

C56H89N15O11

1148.4

GLP-1(28-36)amide acetate(1225021-13-5 Free base)

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years