“…Insulin resistance, together with inflammatory status, might occur due to excess nutritional fructose and affect the intestinal microbiota [1,2]. In our previous studies, we showed that high-fructose intake changed the expression levels of insulin signaling effectors, such as insulin receptor (IR), insulin receptor substrates (IRS-1 and IRS-2), protein kinase B (AKT), or endothelial nitric oxide synthase (eNOS), as well as activated inflammatory markers in blood vessel, adipose tissue, liver, and testis of rats [3,4,5,6,7,8]. In studies with kidney tissue of high-fructose-fed rats, reduced expression or phosphorylation of IR, IRS-1, and AKT, as well as overproduction of cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNF-α), indicated that there is a connection between inflammation and impaired insulin signaling [9,10].…”