Abstract
Non-alcoholic fatty liver disease is a main complication of type 2 diabetes. Isoquercitrin are employed for antidiabetic therapies, but the effects on liver function and the hepatocytes are unclear. The aim of this study was to investigate the effects of isoquercitrin on the T2DM-induced hepatic injury in rats. Isoquercitrin (10 mg/kg/d, 30 mg/kg/d), sitagliptin phosphate (10 mg/kg/d) was given orally for 21 days. The administration of isoquercitrin at 10 mg/kg/d and 30 mg/kg/d showed a dose dependent. Compare to the negative control (treated with saline), rats medicated with isoquercitrin (30 mg/kg/d) and sitagliptin phosphate (10 mg/kg/d) improved the clinical symptoms, FBG and glucose tolerance, reduced serum ALT, AST and IR, but increased TP, Alb, SOD, GSH, MDA, HDL-C, INS and GLP-1. On histology, Rats of these to groups presented nearly normal liver tissue and Langerhans, degeneration, necrosis and apoptosis were markedly reduced. Instead, hepatocytes showed regenerate. These two groups also showed significant increase in mRNA expression of PKA, AKT, PKCa, InsR and PI3K, and a decrease in DPP-IV mRNA level. These results indicated that treatment with isoquercitrin protects against hepatic injury by T2DM.
Highlights
Diabetes mellitus is a chronic metabolic disorder, characterized by hyperglycemia
Compare to the negative control, rats medicated with isoquercitrin (30 mg/kg/d) and sitagliptin phosphate (10 mg/kg/d) improved the clinical symptoms, fasting blood glucose (FBG) and glucose tolerance, reduced serum ALT, AST and insulin resistance (IR), but increased Total protein (TP), Alb, Superoxide dismutase (SOD), GSH, MDA, High-density lipoprotein cholesterol (HDL-C), INS and glucagonlike peptide-1 (GLP-1)
Results showed that isoquercitrin increased the mRNA expression of PKA, AKT, PKCα, InsR and PI3K, and reducing that of DPP-IV in the positive group significantly, followed by the high dose group and the low dose group
Summary
Diabetes mellitus is a chronic metabolic disorder, characterized by hyperglycemia (fasting state>7 mmol/L). Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes, accounts for 90% of the patients. The mechanisms of T2DM are the insulin resistance (IR) of liver and muscle. Most T2DM patients manifested severe hepatic steatosis [1]. Non-alcoholic fatty liver disease (NAFLD) is a clinicopathologic syndrome, recognized as one of the most common causes of liver damage, including hepatic steatosis [2]. Alterations in hepatic metabolism lead to overproduction of glucose and lipids, which in turn abet development of glucose intolerance and dyslipidemias to induce T2DM [3]. Patients with NAFLD increased about 5-fold of the incidence of T2DM [4]. While T2DM are the strongest predictors of NAFLD, more than 70% patients suffered NAFLD [5]
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