Results exhibited that probiotic intake in TLR2−/− mice via enhancing lipopolysaccharides concentration, TLR/JNK pathway activation, ER stress, and downregulation of insulin signaling in both in both liver and muscle tissue [55] and increasing FGF-21 expression that led to activation of butyrate-mediated PPARα, enhance of adipose tissue adiponectin expression could improve metabolic disorders and prevent obesity, insulin resistance and hepatic steatosis in mice with metabolic syndrome [55, 56]. The gene discussed is TLR2; the disease is metabolic syndrome.