Oyster hydrolysate ameliorates ethanol diet‐induced alcoholic fatty liver by regulating lipid metabolism in rats

Summary We evaluated the effect of oyster hydrolysate, which was prepared using transglutaminase, protamex and neutrase (TGPN), on alcoholic fatty liver. Sprague–Dawley rats were fed a diet containing 5% (v/v) ethanol or an isocaloric amount of dextrin–maltose for 6 weeks and orally administered TGPN or silymarin for another 4 weeks. TGPN significantly decreased the liver index (liver weight/body weight), serum and hepatic lipid levels and increased the serum adiponectin level. Based on histological analysis, TGPN reduced the number of lipid droplets and lipid accumulation in liver tissue. TGPN enhanced the expression of AMP‐activated protein kinase and activated its downstream pathway which controls lipid metabolism. Additionally, TGPN decreased the levels of liver function markers (aspartate aminotransferase and alanine aminotransferase) and tumour necrosis factor alpha. Consequently, TGPN ameliorated alcoholic fatty liver by inhibiting fatty acid and cholesterol synthesis, promoting fatty acid oxidation and decreasing liver cell damage. In this study, we investigated Oyster hydrolysate ameliorates ethanol diet–induced alcoholic fatty liver by regulating AMPK pathway and adiponectin.