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Background  The incidence of metabolic syndrome linked to dyslipidemia and insulin resistance has increased; thus, studies must be conducted to elucidate this phenomenon. The present study aimed to investigate the protective effects of chokeberry and dried jujube diet on high-fat and high-fructose diet-induced dyslipidemia in mice.    Methods  Male C57BL/6 J mice were divided into five groups: ND, mice fed normal diet and tap water; HFFD, mice fed 60% high-fat and 10% fructose diet (HFFD) in tap water; HFFD+C, mice fed HFFD with 1% chokeberry powder; HFFD+J, mice fed HFFD with 1% jujube fruit powder; and HFFD+M, mice fed HFFD with 0.5% chokeberry + 0.5% jujube fruit powder mixture.    Results  After 10 weeks of dietary treatment, chokeberry and dried jujube fruits reduced HFFD-induced weight gain and central obesity and decreased liver weight and abdominal and epididymal fat mass. Furthermore, such fruits attenuated HFFD-induced dyslipidemia; decreased triglyceride, total cholesterol, non-high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and very-low-density lipoprotein-cholesterol levels. Insulin resistance was improved via the consumption of dietary chokeberry and dried jujube fruits according to various indicators (serum insulin level, fasting blood glucose level, homeostatic model assessment-insulin resistance score, and oral glucose tolerance test value). These treatments were found to lower serum triglyceride levels. Moreover, the consumption of chokeberry and dried jujube changed the hepatic protein expression of insulin receptor, insulin receptor substrate 1, phosphoinositide 3-kinase, Akt, and catalase, which are associated with insulin resistance.    Conclusions  Chokeberry and dried jujube could be used in the management of dyslipidemia and insulin resistance associated with metabolic syndrome by reducing risk parameters in mice with HFFD.

nutrition and metabolism

Dietary chokeberry and dried jujube fruit attenuates high-fat and high-fructose diet-induced dyslipidemia and insulin resistance via activation of the IRS-1/PI3K/Akt pathway in C57BL/6 J mice