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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

1415.68

C₆₄H₁₁₀N₂₀O₁₆

1096485-24-3

LRQFLQKSLAAAA-NH2

Room temperature in continental US; may vary elsewhere.

H₂O

Peptide Solubility and Storage Guidelines:

1.;;Calculate the length of the peptide.

2.;;Calculate the overall charge of the entire peptide according to the following table:

3.;;Recommended solution:

• [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.

For studies examining hormone secretion from cell lines, INS 832/13 or αTC1-9 cells are plated in 96- or 24-well plates at a density of 0.25×10⁵ cells/well or 1.0×10⁵ cells/well in complete medium. The day of the experiment, cells are washed in PBS and allowed to preincubate in low- or high-glucose KRB buffer for 1 h in the presence or absence of Neuronostatin-13 human. Hormone secretion is performed using a 2-h static incubation. Supernatants are collected, and insulin or glucagon content is determined^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

3-month-old adult male C57BL/6 mice are used and housed in a temperature-controlled environment (22.8±2.0°C, 45 to 50% humidity) with a 12:12h light/dark cycle with free access to food and tap water. For Neuronostatin-13 human challenge in vivo, 3-month-old adult C57BL/6 male mice are randomly divided into two groups and to receive Neuronostatin-13 human (50 μg/kg, i.p.). Cardiac function is evaluated at 3-, 6-, 12- and 18-hr after Neuronostatin-13 human treatment in the first group of animals^[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [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.