Neuronostatin-13human是一种由生长抑素基因编码的由13个氨基酸组成的肽激素，在调节激素和心脏功能中起着重要作用。
CAS：1096485-24-3
分子式：C64H110N20O16
分子量：1415.68
纯度：98%
存储：Store at -20°C

Background:

Neuronostatin-13 human is a 13-amino acid peptide hormone encoded by the somatostatin gene and plays an important role in the regulation of hormonal and cardiac function.

Neuronostatin-13 human is a 13-amino acid peptide hormone encoded by the somatostatin gene and plays an important role in the regulation of hormonal and cardiac function. Treatment with Neuronostatin-13 human (1,000 nM) enhances low-glucose-induced glucagon release compare with islets treated with control medium alone. Treatment with Neuronostatin-13 human for 1 h leads to a significant increase in the accumulation of glucagon mRNA compare with vehicle-treated control cells. In αTC1-9 α-cells, treatment with 100 nM Neuronostatin-13 human leads to an increase in phosphorylated PKA at 30 and 40 min[1].

Infusion with Neuronostatin-13 human delays glucose clearance in the rat model, such that blood glucose levels in Neuronostatin-13 human-treated animals are significantly higher at 1 and 10 min following intra-arterial injection of a glucose bolus[1]. Chocardiographic measurement reveals a remarkable drop in heart rate after 3-, 6- and 12-hr of Neuronostatin-13 human challenge. In addition, Neuronostatin-13 human treatment significantly decreases left ventricular end-systolic diameter (LVESD) and fractional shortening without affecting left ventricular end-diastolic diameter (LVEDD) between 6 and 12 hrs following Neuronostatin-13 human challenge, the effect of which returns to basal level 18-hr after Neuronostatin-13 human treatment[2].

[1]. Salvatori AS, et al. Neuronostatin inhibits glucose-stimulated insulin secretion via direct action on the pancreatic α-cell. Am J Physiol Endocrinol Metab. 2014 Jun 1;306(11):E1257-63. [2]. Zhu X, et al. Neuronostatin attenuates myocardial contractile function through inhibition of sarcoplasmic reticulum Ca2+-ATPase in murine heart. Cell Physiol Biochem. 2014;33(6):1921-32.