Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
Advanced search 
Year : 2018  |  Volume : 14  |  Issue : 56  |  Page : 344-350

The effects of emodin on insulin resistance in KKAy mice with diabetes mellitus

1 Department of Endocrinology, The First Affiliated Hospital of Liaoning Medical University, Liaoning, China
2 College of Basic Medicine, Jinzhou Medical University, Jinzhou, China

Correspondence Address:
Liu Xuezheng
3-40, Songpo Road, Jinzhou, Liaoning Province
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_362_17

Rights and Permissions

Background: Emodin can ameliorate insulin resistance in diabetes mellitus (DM), but the molecular mechanisms are still uncertain. Objective: The objective of this study is to identify the potential molecular mechanisms of emodin-mediated type 2 DM treatment. Methods: We treated the type 2 diabetic KKAy mice with emodin in different doses. Biochemistry data were collected, and the expression of peroxisome proliferator activated receptor γ (PPARγ) and Glucose transporter (GLUT)-2/4 were examined in liver, muscle, and adipose tissues using immunohistochemistry and reverse transcriptase polymerase chain reaction. The expression of IRS-1, PI3K, pAkt-ser473, and FoxO1 were also tested in these tissues. Results: Our data demonstrated that the levels of cholesterol, higher fasting plasma glucose, total cholesterol, total triacylglycerol, low-density lipoprotein cholesterol, free fatty acid, C creative protein, and tumor necrosis factor-α (P < 0.05), lower high-density lipoprotein, and insulin sensitivity index (P < 0.05) were ameliorated by emodin in a dose-dependent manner (P < 0.05). In addition, emodin was also identified to improve insulin sensitivity in KKAy diabetic mice (P < 0.05). In DM, the expression of PPARγ and GLUT-2 was down-regulated in liver (P < 0.05) as well as in muscle and adipose tissues (P < 0.05) when compared with the controls. However, the decreased levels were subject to emodin treatment in a dose-dependent manner. Meantime, emodin was identified to up-regulate the expression of IRS-1, PI3K, Akt-ser473 (P < 0.05), while FoxO1 (P < 0.05) was down-regulated. Conclusion: These results suggest that emodin represents a promising target to improve insulin sensitivity by enhancing liver glucose utilization, glucose uptake of muscle, and fat through IRS/PI3K/Akt/FoxO1 pathway. Abbreviations used: DM: Diabetes mellitus; PPARγ: Peroxisome proliferator activated receptor γ; GLUT: Glucose transporter; IRS: Insulin receptor substrate; PI3K: Phosphatidylinositide 3 kinase; Akt(PKB): Protein kinase; FoXO1: Fork head box protein O1.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded125    
    Comments [Add]    

Recommend this journal