The Regulatory Effect of Neutral Polysaccharide from Acanthopanax trifoliatus (L.) Merr on Intestinal Disaccharidase in Type 2 Diabetic Mice
Article
Figures
Metrics
Preview PDF
Reference
Related
Cited by
Materials
Abstract:
This study investigated the regulatory effect of neutral polysaccharide from Acanthopanax trifoliatus (L.) Merr (ATP1-1) on intestinal disaccharidase in type 2 diabetic mice. A Type 2 diabetic mouse model was established through the induction by high-fat diet combined with streptozotocin (STZ). All diabetic mice were divided into 4 groups: model group, metformin group [185 mg/(kg·d)], high-dose ATP1-1 group [80 mg/(kg·d)], and low-dose ATP1-1 group [40 mg/(kg·d)]. Normal group was also set separately. The mice were given continuous intragastric administration for 8 weeks, during which Fasting blood glucose (FBG), glucose, sucrose and maltose tolerance were determined. After the last administration, in vivo and in vitro disaccharidase activities as well as the mRNA expressions of sucrase-isomaltase (SI) and glucagon-like peptide-1 (GLP-1) were evaluated. The results showed that compared with the model group, the FBG of the mice in high-dose ATP1-1 and low-dose ATP1-1 groups decreased by 27.06% and 19.96%, respectively (p<0.01), and the glucose, sucrose and maltose tolerance of the diabetic mice were significantly improved (p<0.01). In vivo experiments showed that the inhibition rates of high-dose ATP1-1 on the sucrase of the duodenum, jejunum and ileum were 48.29%, 75.09% and 31.41%, respectively, with the inhibition rates against the corresponding maltases being 26.23%, 18.34%, and 34.18%, respectively. In vitro experimental results showed that the IC50 of ATP1-1 on the duodenal sucrase and maltase were 3 381.00 μg/mL and 226.50 μg/mL, respectively. Meanwhile, ATP1-1 could up-regulate GLP-1 mRNA expression and down-regulate SI mRNA expression (p<0.01). Therefore, ATP1-1 can inhibit the activity and expression of intestinal disaccharidase, and promote the expression of GLP-1 to improve the hyperglycemia state of type 2 diabetic mice.
