Abstract
To investigate the effects of Astragalus membranaceus and Potentilla discolor mixture (APM) on insulin resistance (IR) and mRNA expressions of IR-related genes, including phosphatidylinositol 3-kinase (PI3-K), phosphoenolpyruvate carboxykinase (PEPCK) and peroxisome proliferator-activated receptor γ coactivator 1 (PGC1) in KKAy mice with early type 2 diabetes and to explore the gene regulation mechanisms of AMP. After giving short-term high-fat and high-calorie diet to induce type 2 diabetes, male KKAy mice were randomly divided into model and APM groups. Nine C57BL/6J mice were used as normal control in addition. The mice in the APM group were treated with 830 g/L of the APM liquid by gastric infusion while the mice in the model group and the normal control group were given 0.05% sodium carboxymethyl cellulose at a dose of 0.1 mL/g body weight once per day. After four weeks, fasting plasma glucose (FPG) was tested using tail vein blood. Fasting serum insulin (FINS) was tested by radioimmunoassay. Insulin sensitivity index (ISI) was calculated as the natural logarithm of the product of FPG and FINS. The mRNA expressions of PI3-K, PEPCK and PGC1 in liver tissues were tested by real-time fluorescence quantitative polymerase chain reaction assay. Both the levels of FPG and FINS in the model group and the APM group were increased, while the ISI values were decreased when compared to those of the normal control group (P<0.01). The level of FPG in the APM group was decreased, while ISI was increased when compared to those of the model group (P<0.05). All of the mRNA expressions of PI3-K, PEPCK, and PGC1 in liver tissue of the model group were decreased compared with the normal control group (P<0.01). The mRNA expressions of PI3-K and PGC1 in the liver tissue of the APM group were higher than those in the model group (P<0.05). APM can improve the insulin resistance of mice with type 2 diabetes. The mechanism may be related to increasing the mRNA expressions of PI3-K and PGC1 in the liver tissue.
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