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

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 P P P P P P P 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.