PUBLICATION

A synthetic Nitraria alkaloid, isonitramine protects pancreatic β-cell and attenuates postprandial hyperglycemia

Authors
Kwon, S.J., Hwang, S.J., Jung, Y., Park, H.G., Kim, M.H., Park, Y., Lee, H.J.
ID
ZDB-PUB-170414-9
Date
2017
Source
Metabolism: clinical and experimental   70: 107-115 (Journal)
Registered Authors
Keywords
Diabetes mellitus, Insulin, Isonitramine, PEPCK, α-amylase, α-glucosidase
MeSH Terms
  • Alkaloids/isolation & purification
  • Alkaloids/pharmacology*
  • Aniline Compounds/isolation & purification
  • Aniline Compounds/pharmacology*
  • Animals
  • Carbohydrate Metabolism/drug effects
  • Cell Line
  • Cricetinae
  • Glycoside Hydrolase Inhibitors
  • Humans
  • Hyperglycemia/drug therapy*
  • Hypoglycemic Agents/isolation & purification
  • Hypoglycemic Agents/pharmacology
  • Insulin-Secreting Cells/drug effects*
  • Nitrobenzenes/isolation & purification
  • Nitrobenzenes/pharmacology*
  • Phosphoenolpyruvate Carboxykinase (ATP)/drug effects
  • Plant Extracts/chemistry
  • Protective Agents/isolation & purification
  • Protective Agents/pharmacology
  • Rats
  • Swine
  • Zebrafish
PubMed
28403934 Full text @ Metab. Clin. Exp.
Abstract
The extracts of Nitraria genus are composed of Nitraria alkaloids and have been used traditionally as a hypoglycemic medicine. However, the efficacy and precise mechanism of Nitraria alkaloids remain largely unknown.
Previously, we reported the total synthesis of (+)-isonitramine, one of Nitraria alkaloids. In this study, we investigated the anti-diabetic potential of isonitramine in diabetes mellitus and its underlying molecular mechanism in carbohydrate catabolism in vitro and in vivo.
Isonitramine exerted significant inhibitory effect on α-glucosidases but not α-amylase in vitro. In zebrafish, isonitramine alleviated the streptozotocin (STZ)-induced postprandial hyperglycemia and protected the pancreatic damages against alloxan-induced oxidative stress in vivo. Also, isonitramine induced insulin without any toxicities and downregulated phosphoenolpyruvate carboxykinase (PEPCK), which catalyzes the first committed step in gluconeogenesis.
Taken together, isonitramine inhibited α-glucosidase activity and PEPCK expression, while increased insulin expression, resulting in attenuating the postprandial hyperglycemia. Also, isonitramine protected the pancreas from ROS-mediated toxicities. Therefore, isonitramine may be a new drug candidate for the treatment of diabetes mellitus.
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