Directly enters the glycolytic pathway, bypassing the major control point by which glucose enters glycolysis. This unregulated carbon source provides glycerol-3-phosphate and acetyl-CoA for hepatic lipogenesis, increasing the hepatic pool of free fatty acids. In addition, fructose neither suppresses ghrelin nor stimulates insulin or leptin to inhibit appetite. According to a previous study, the prevalence of NAFLD in Taiwan ranges from 11-41%. Of the NAFLD patients, 6-13% were diagnosed with NASH. NAFLD has a severe impact on health that substantially increases when combined with obesity, diabetes, and the metabolic syndrome. The presence of HFCS in beverages plays an important role in the progression of hepatic manifestations of the metabolic syndrome, including obesity, insulin resistance, NAFLD, and NASH. In 1998, Day and James proposed the “double hit” hypothesis. The first hit refers to the abnormal accumulation of lipids, especially triglycerides, in the liver. With the dysregulation of liver lipid homeostasis, free fatty acids continue to be transported to the liver, resulting in a decreased capacity for b-oxidation of fats. In addition, most studies suggest that NASH is related to inflammation and insulin resistance. Further studies have shown that insulin resistance may lead to overexpression of the lipoprotein lipase gene, thereby enabling continuous generation of free fatty acids in the liver. Most patients may simply have a fatty liver with no associated inflammation. However, the “second hit” induces inflammatory responses, including abnormal inflammatory cytokine production and oxidative stress response. Reactive oxygen species activate redox-sensitive kinases, thereby activating IkappaB kinase beta, inducing nuclear factor-kB activation, and further increasing the expression of TNF-a and production of cytokines by other inflammatory cells, leading to inflammation of the liver. Therefore, improvement of hepatic lipid metabolism and accumulation in “first-hit” and alleviating inflammation, insulin resistance and oxidative stress in “secondhit” have been shown the therapeutic potential in preventing the progression of HMMS. Lactoferrin is a single chain glycoprotein consisting of 700 amino acid residues, with a molecular weight of 76-80 kD. It plays a variety of physiological roles, and mediates antibacterial, antiviral, and anti-inflammatory effects. Lactoferrin exerts an antibacterial effect by binding iron ions, which reduces the iron-dependent growth of bacteria such as E. coli. However, lactoferrin also acts as an iron donor to promote the growth of beneficial bacteria, such as Lactobacillus and Bifidobacterium. Inflammation or infection due to stimulation of phagocytes and release of cytokines further increases neutrophil infiltration. Lactoferrin is able to bind lipopolysaccharides, and is thereby able to reduce the LPS-driven inflammatory response.