Effects of Genistein on PCOS-IR Rats through Adiponectin and RBP4 Pathway
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Abstract:
A rat model of polycystic ovary syndrome with insulin resistance (PCOS-IR) was established by administering subcutaneous injections of dehydroepiandrosterone (DHEA) and human chorionic gonadotropin (HCG) and a high-fat diet to study the effects of genistein (Gen) on insulin resistance through adiponectin (APN) and retinol binding protein-4 (RBP4) pathways. Rats were randomly divided into the control group, model group, low-, medium-, and high-dose Gen treatment groups, and metformin treatment group according to their body weights. Each group had eight rats. After 21 days of continuous treatment, the levels of Fasting Blood Glucose (FBG), Fasting insulin (Fins), APN, and RBP4 were measured, and the expression of APN- and RBP4-related genes and proteins in the ovarian tissue was analyzed. The results showed that in comparison with the model group, the medium-dose Gen treatment group had a significantly decrease of 13.95% in the FBG. Fins levels of the medium- and high-dose Gen treatment groups decreased by 45.80% and 51.80%, respectively, as compared to the level in the model group. The insulin resistance index of the high-dose group significantly reduced by 57.20%. Serum APN and Adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) levels of the medium-dose group were significantly higher by 69.43% and 36.57%, respectively, and RBP4 level of the high-dose group was significantly lower by 59.01% than those in the model group. The level of phosphoenolpyruvate carboxykinase (PEPCK) of the medium-dose group remarkably reduced by 22.63%. The gene and protein expression levels of APPL1, AMP-activated protein kinase (AMPK), and p-AMPK in the ovarian tissue of the medium- and high-dose groups considerably increased, but those of RBP4 and PEPCK significantly decreased. Thus, medium and high doses (20 and 30 mg/kg) of Gen can effectively improve glucose metabolism and insulin resistance in PCOS-IR rats through adiponectin and RBP4 pathways.
