The Regulatory Effect of Lactoferrin on High-Fructose Induced Nonalcoholic Fatty Liver Disease in Murine Model

• Main Authors: Yi-Chieh Li, 李宜潔
• Other Authors: Chang-Chi Hsieh
• Format: Others
• Language: zh-TW
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/89276179927449272658

碩士 === 東海大學 === 畜產與生物科技學系 === 101 === The increase in fructose consumption is paralleled by a higher incidence of obesity and associate to metabolic syndrome including hypertriglyceridemia, fatty liver, hypertension, insulin resistance and diabetes mellitus. In recent years, several studies had been published that implicate subclinical chronic inflammation as an important pathogenic factor in the development of fatty liver. The most important reasons will be the hyperglycemia, high blood glucose, causes oxidative stress and leading inflammation. High fructose diet modulated the distribution of gut microbes and increased Gram negative bacteria proliferation further increased lipopolysaccharide (LPS) releasing. Lactoferrin, an iron-binding glycoprotein, regulated several physiological functions such as antimicrobial activity, especially in Gram negative bacteria. Previous studies indicated lactoferrin reduced serum triglyceride and down-regulated inflammation in rat. The purpose of this study was to investigate that lactoferrin protects against the onset of non-alcoholic fatty liver disease via anti-inflammation in high-fructose administered murine model. Our results indicated high-fructose diet stimulated intestinal bacterial overgrowth and increased intestinal permeability, subsequently leading to endotoxin in blood circulation and liver. Immunohistochemical staining of Toll-like receptor-4 (TLR-4) indicated lactoferrin could modulate LPS mediated inflammatory cascade. These inflammatory response in adipokines include interleukin-1β (IL-1β), IL-6, IL-33, tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1), thymic stromal lymphopoietin (TSLP) and adiponectin. Furthermore, lactoferrin could reduce serum and hepatic triglycerides, and lipid accumulation in liver, finally reduced hepatic damage and decreased serum alanine aminotransferase (ALT) release. These beneficial effects of lactoferrin were related to the decreased LPS induced inflammatory cascade in liver and also significantly lowered liver weight that ameliorated fatty liver by decrease of triglyceride and cholesterol syntheses in activating hepatic steatosis. These findings suggest that lactoferrin had the potential to improve nonalcoholic fatty liver disease in murine model.