Abstract

In the present study, the hypoglycemic, hypolipidemic, and antioxidative effects of metformin (MET) combined with Jiang Tang Xiao Ke (JTXK) granule derived from the “Di Huang Tang” were evaluated in mice with type 2 diabetes mellitus (DM) induced by high-fat diet/streptozotocin. DM mice were orally treated with MET (0.19 g/kg) either alone or combined with different doses (1.75, 3.5, or 7 g/kg) of JTXK for 4 weeks. Results showed that the serum and hepatic glucose, lipids, and oxidative stress levels were elevated in DM mice, when compared with the normal mice. MET treatment decreased FBG and serum glucagon levels of DM mice. Combination treatment with MET and JTXK 3.5 g/kg increased the hypoglycemia and insulin sensitivity at 4 weeks when compared with the DM mice treated with MET alone. However, neither MET nor MET/JTXK treatment could completely reverse the hyperglycemia in DM mice. JTXK enhanced the serum triglyceride (TG) and hepatic lipid-lowering effect of MET in a dose-dependent manner in DM mice. JTXK 1.75 and 3.5 g/kg improved the hepatoprotective effect of MET in DM mice. Synergistic effect of combination treatment with MET and JTXK on antioxidant stress was also found in DM mice compared with MET alone.

Highlights

  • Diabetes mellitus (DM) is a metabolic disease with decreased glucose transport into muscle and fat cells and increased hepatic glucose output resulting from dysfunction in insulin secretion or resistance to its activity [1, 2]

  • The same dose of MET combined with Jiang Tang Xiao Ke (JTXK) 1.75, 3.5, and 7 g/kg lowered fasting blood glucose (FBG) levels by 25.21, 36.63, and 37.81%, respectively, at 2 weeks after MET/JTXK treatment, when compared with DM group mice, but had no statistical differences (p > 0.05) in comparison with mice treated with MET alone

  • Compared with MET alone group, MET combined with JTXK 3.5 g/kg treatment can significantly reduce the level of FBG in DM mice (Table 1)

Read more

Summary

Introduction

Diabetes mellitus (DM) is a metabolic disease with decreased glucose transport into muscle and fat cells and increased hepatic glucose output resulting from dysfunction in insulin secretion or resistance to its activity [1, 2]. One of the most common complications of DM is nonalcoholic fatty liver disease (NAFLD), a risk factor for the development of type 2 diabetes [4, 5]. Both experimental and clinical data have demonstrated that oxidative stress is involved in DM and DM secondary complications such as NAFLD and NASH [11,12,13]. Oxidative stress and diminished antioxidants within the liver are the key features of NAFLD/NASH while insulin resistance is largely responsible for the development of NAFLD/NASH, which causes hepatic steatosis [15]

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call