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Molecules 2016, 21(3), 279; doi:10.3390/molecules21030279

1-Deoxynojirimycin Alleviates Liver Injury and Improves Hepatic Glucose Metabolism in db/db Mice

1
College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
2
Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, Nanjing 210023, China
*
Author to whom correspondence should be addressed.
Academic Editor: Derek J. McPhee
Received: 3 January 2016 / Revised: 21 February 2016 / Accepted: 23 February 2016 / Published: 27 February 2016
(This article belongs to the Section Medicinal Chemistry)
View Full-Text   |   Download PDF [5950 KB, uploaded 27 February 2016]   |  

Abstract

The present study investigated the effect of 1-Deoxynojirimycin (DNJ) on liver injury and hepatic glucose metabolism in db/db mice. Mice were divided into five groups: normal control, db/db control, DNJ-20 (DNJ 20 mg·kg−1·day−1), DNJ-40 (DNJ 40 mg·kg−1·day−1) and DNJ-80 (DNJ 80 mg·kg−1·day−1). All doses were treated intravenously by tail vein for four weeks. DNJ was observed to significantly reduce the levels of serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and liver TG, as well as activities of serum alanine aminotransferase (ALT), and aspartate transaminase (AST); DNJ also alleviated macrovesicular steatosis and decreased tumor necrosis factor α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6) levels in liver tissue. Furthermore, DNJ treatment significantly increased hepatic glycogen content, the activities of hexokinase (HK), pyruvate kinase (PK) in liver tissue, and decreased the activities of glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK). Moreover, DNJ increased the phosphorylation of phosphatidylinositol 3 kinase (PI3K) on p85, protein kinase B (PKB) on Ser473, glycogen synthase kinase 3β (GSK-3β) on Ser9, and inhibited phosphorylation of glycogen synthase (GS) on Ser645 in liver tissue of db/db mice. These results demonstrate that DNJ can increase hepatic insulin sensitivity via strengthening of the insulin-stimulated PKB/GSK-3β signal pathway and by modulating glucose metabolic enzymes in db/db mice. Moreover, DNJ also can improve lipid homeostasis and attenuate hepatic steatosis in db/db mice. View Full-Text
Keywords: 1-Deoxynojirimycin; db/db mice; liver; lipid metabolism; hepatic glucose metabolism; hepatic glycogen; glucose metabolic enzymes; hepatic insulin sensitivity; PKB/GSK-3β 1-Deoxynojirimycin; db/db mice; liver; lipid metabolism; hepatic glucose metabolism; hepatic glycogen; glucose metabolic enzymes; hepatic insulin sensitivity; PKB/GSK-3β
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Liu, Q.; Li, X.; Li, C.; Zheng, Y.; Wang, F.; Li, H.; Peng, G. 1-Deoxynojirimycin Alleviates Liver Injury and Improves Hepatic Glucose Metabolism in db/db Mice. Molecules 2016, 21, 279.

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