A synthetic Nitraria alkaloid, isonitramine protects pancreatic beta-cell and attenuates postprandial hyperglycemia
- Authors
- Kwon, So Jung; Hwang, Su Jung; Jung, Yeonghun; Park, Hyeung-geun; Kim, Mi-hyun; Park, Yohan; Lee, Hyo-Jong
- Issue Date
- May-2017
- Publisher
- W B SAUNDERS CO-ELSEVIER INC
- Keywords
- Isonitramine; Diabetes mellitus; alpha-glucosidase; alpha-amylase; PEPCK; Insulin
- Citation
- METABOLISM-CLINICAL AND EXPERIMENTAL, v.70, pp.107 - 115
- Journal Title
- METABOLISM-CLINICAL AND EXPERIMENTAL
- Volume
- 70
- Start Page
- 107
- End Page
- 115
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6144
- DOI
- 10.1016/j.metabol.2017.02.002
- ISSN
- 0026-0495
- Abstract
- Objective. 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. Methods. Previously, we reported the total synthesis of (+)-isonitramine, one of Nitraria alkaloids. In this study, we investigated the and-diabetic potential of isonitramine in diabetes mellitus and its underlying molecular mechanism in carbohydrate catabolism in vitro and in vivo. Results. Isonitramine exerted significant inhibitory effect on alpha-glucosidases but not alpha-amylase in vitro. In zebrafish, isonitramine alleviated the streptozotocin (SIZ)-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 caxboxykinase (PEPCK), which catalyzes the first committed step in gluconeogenesis. Conclusion. Taken together, isonitramine inhibited a-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. (C) 2017 Elsevier Inc. All rights reserved.
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