Taken together, this report gives the first account of glycolipid binding preferences of Stx2 variants and the role of B-subunits in these interactions. The knowledge of receptor binding preferences of Stx variants will not only SCH 442416 provide understanding of the different toxicities of these highly related variants but it will also provide a means to detect and differentiate these variants during a STEC outbreak. Non-alcoholic fatty liver disease represents a spectrum of diseases ranging from hepatic steatosis to steatohepatitis and cirrhosis. The hallmark of NAFLD is excess triglyceride accumulation within hepatocytes. NAFLD is the most common liver disease in Western countries; approximately one third of all Western populations are affected, and the prevalence of these diseases continues to progressively increase. Emerging evidence suggests that NAFLD is the hepatic manifestation of metabolic syndrome and is a risk factor for cardiovascular diseases. Antihyperlipidemic drugs are recommended as part of the treatment for L-733,060 hydrochloride patients with NAFLD. Fibrates are synthetic ligands of peroxisome proliferator-activated receptor a, and they serve as first-line drugs for reducing serum triglyceride levels. The lipid-lowering action of fibrates in the blood is mediated through the activation of PPARa and lipoprotein lipase and the suppression of apolipoprotein C-III, among other proteins.. Theoretically, fibrates might be beneficial for the treatment of NAFLD. However, no definitive conclusion on the efficacy of PPARa agonists in the treatment of NAFLD can be drawn based on the available clinical data. Some studies have suggested that PPARa activation might have protective and therapeutic effects against NAFLD, while others have reported contrasting findings. Fenofibrate, one of the most commonly used fibrates, was reported to exert no beneficial effect on liver steatosis, as assessed using MRI. In 16 patients with biopsy-confirmed NAFLD, 48 weeks of therapy with fenofibrate did not reveal any significant change in the grade of steatosis, lobular inflammation, fibrosis, or the NAFLD activity score when determined by liver histology. Another study investigated liver biopsies before and after 12 months of clofibrate treatment and revealed no improvement in the histological grade of steatosis, inflammation, or fibrosis. We conducted preliminary experiments exploring the effect of fenofibrate as a monotherapy on NAFLD in several patients. Notably, MRI did not reveal any significant change in the steatosis score.