PUBLICATION

Corosolic acid isolated from Eriobotrya japonica leaves reduces glucose level in human hepatocellular carcinoma cells, zebrafish and rats

Authors
Xu, S., Wang, G., Peng, W., Xu, Y., Zhang, Y., Ge, Y., Jing, Y., Gong, Z.
ID
ZDB-PUB-190315-3
Date
2019
Source
Scientific Reports   9: 4388 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Carcinoma, Hepatocellular/blood
  • Carcinoma, Hepatocellular/drug therapy*
  • Carcinoma, Hepatocellular/metabolism
  • Eriobotrya/chemistry*
  • Glucose/metabolism*
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms/blood
  • Liver Neoplasms/drug therapy*
  • Liver Neoplasms/metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Triterpenes/isolation & purification
  • Triterpenes/pharmacology*
  • Triterpenes/therapeutic use*
  • Zebrafish
PubMed
30867526 Full text @ Sci. Rep.
Abstract
Type 2 diabetes (T2D) with high morbidity and mortality is characterized by abnormal glucose and lipid metabolism due in part to insulin resistance in liver, which lead to elevated hyperglycemia and hyperlipidemia. This study sough to explore the effects of corosolic acid (CA) in different T2D models and explored the underlying mechanism. Separated from Eriobotrya japonica leaves, CA purity was above 95% measured by a HPLC method. Compared with cAMP and DEX induced T2D HepG2 model, CA significantly stimulated glucose consumption and improved glycogen accumulation by inhibiting PEPCK mRNA expression. And in cAMP and DEX induced T2D zebrafish model, CA reduced glycogen degradation and increased glucose consumption by regulating some key enzymes in carbon metabolism including GLUT1, GLUT2, GLUT3, LDHA, LDHB, GP, G6Pase, GYS1, and PFKFB3. In addition, insulin receptor signals were also involved in CA-regulated hypoglycemic action. Furthermore, in STZ-induced T2D rat model, compared with diabetic control groups, CA remarkably downregulated the levels of serum lipid, blood glucose, ICAM-1, malonaldehyde and insulin resistance index, while upregulated SOD activity and impaired glucose tolerance. In a conclusion, CA can regulate glucose and lipid metabolic adaptation in T2D like HepG2, zebrafish and rat models partly through reducing inflammation and oxidative stress and suppressing PEPCK.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping