Article · Volume 14, Issue 56 · pp. 344–350

The Effects of Emodin on Insulin Resistance in KKAy Mice with Diabetes Mellitus

Song Bing¹, Zhang Haoqiang¹, Ma Chunyu², Yu Yali¹, Wang Jing¹, Gao Yumeng¹, Zheng Hongwei¹, Liu Xuezheng²

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

Abstract

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.

Keywords: Emodin; glucose transporter; insulin sensitivity; KKAy diabetic mice; peroxisome proliferation‑activated receptor‑γ; phosphatidylinositol‑3 kinase

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