Abstract：Objective: In order to utilize the waste effectively in Katsuwonus pelamis processing, we studied the effects of the enzymatic hydrolyte of Katsuwonus pelamis liver (KPLH) on lipid metabolism in rats. Material: Fresh Katsuwonus pelamis liver was homogenized and auto- enzymatic hydrolyzed in 25℃ for 12hours. After percolation, the enzymatic hydrolyte of Katsuwonus pelamis liver was freeze-dried. Animal experiment: The Male SD rats were fed high fructose basic diet (AIN 76) for 1 week. Then rats were randomly divided into 3 groups and fed 5% or 10% freeze-dried KPLH containing high fructose basic diet（KPLH group）or high fructose basic diet (control group). After 4 weeks, serum triglyceride (TG), total cholesterol (TC)，high density lipoprotein cholesterol (HDL-C), Free fatty acid (NEFA) levels, and hepatic lipid concentrations (TG, TC) were determined. To resolve the mechanism of lipids lowing effect of KPLH in rats, the activities of key enzymes related in lipids metabolism, malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH), fatty acid synthase (FAS) and carnitin palmitoyl transferase (CPT) were determined. Results: After 4 weeks feeding, KPLH did not affect the food intake, body weight gain, liver weight in rats. The abdominal white adipose tissue weights were lower in KPLH group compared with the control group (no statistical difference, p>0.05). The serum TG levels and atherogenic index (AI) were significantly decreased in KPLH group compared with the control group (P <0.05, P <0.01), and the serum HDL-C levels were significantly up-regulated by KPLH (P <0.05). The concentration of serum total cholesterol was lower in KPLH group than that in control group, but there was not significant difference between KPLH group and control group (p>0.05). On the other hand, KPLH did not alter serum glucose and NEFA levels in rats. Those results showed that the enzymatic hydrolyte of Katsuwonus pelamis liver is beneficial to prevent hyperlipidemia and artheroschlerosis. In liver, KPLH decreased significantly the TG concentration (P <0.001) but not total cholesterol and phospholipids levels. Furthermore, the activities of G6PDH, ME and FAS were decreased by 5% KPLH in liver (P <0.05, P <0.01 and P <0.05). On the other hand, KPLH did not alter the activity of CPT in liver. These suggested that the serum lipids lowing effect of KPLH is related to the down-regulation of hepatic fatty acid synthesis. Conclusion: This study indicated that the KPLH have anti-atherogenic and anti-fatty liver effects by reduced hepatic fatty acid sythesis.