[No authors listed]
Insulin resistance, as a common metabolic disorder, may be caused by dietâinduced obesity. The aim of the present study is to investigate the effects of dioscin on regulating insulin resistance of adipose tissue induced by a highâfat diet (HFD). An animal model was established successfully using C57BL/6J mice with highâfat feeding, followed by treatment with 5, 10 and 20Â mg/kg dioscin through gavage for 18Â weeks, and randomly divided into a control group, a HFD model group and a dioscin group treated with 5, 10 and 20Â mg/kg/day dioscin for 12Â weeks. Histopathological changes in adipose tissues were examined using hematoxylin and eosin staining. Biochemical parameters of the serum were also monitored, including glucose, insulin, total triglyceride, homeostasis model assessment of insulin resistance (HOMAâIR) and adipose insulin resistance (AdipoâIR) levels. Expression of the mRNA and associated proteins of the insulin receptor substrate 1 (IRSâ1)/phosphoinositide 3âkinase (PI3K)/protein kinase B (Akt) pathways were determined using reverse transcriptionâquantitative polymerase chain reaction (RTâqPCR) and western blot analysis, respectively. HOMAâIR and AdipoâIR values of mice fed with a HFD were significantly higher compared with those in the control group (P<0.01). However, dioscin administration significantly decreased HOMAâIR and AdipoâIR values in a doseâdependent manner (P<0.05), suggesting the effects of dioscin on attenuating insulin resistance. RTâqPCR results indicated that the associated genes of the IRSâ1/PI3K/Akt pathway were significantly downregulated by HFD compared with the control group (P<0.05), while dioscin significantly increased the expression of those genes compared with the control group (P<0.05). Similarly, the significant increase in phosphorylated (pâ)IRSâ1/IRSâ1 (P<0.05) and pâAkt/Akt (P<0.05) values were substantially reversed by dioscin treatment. Dioscin pronouncedly mitigated insulin resistance in adipose tissues through the IRSâ1/PI3K/Akt pathway and has potential to be used as a novel therapeutic agent for the therapy of HFDâinduced insulin resistance in adipose tissue.
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