Abstract

Abstract A 10-week growth trial was conducted to examine the effects of dietary cholesterol on feed intake, growth performance and cholesterol metabolism in juvenile turbot ( Scophthalmus maximus L.) (initial body weight 5.18 ± 0.01 g). Five isonitrogenous and isolipidic experimental diets were formulated with supplementation of 0.0, 0.5, 1.0, 1.5 and 2.0% cholesterol, and the final dietary cholesterol concentrations were 0.38, 0.76, 1.30, 1.80 and 2.22%, respectively. WGR of fish fed diets with 1.30, 1.80 and 2.22% cholesterol was significantly higher than that of fish fed the diet with 0.38% cholesterol, but no significant differences of WGR were found among fish fed diets with 1.30, 1.80 and 2.22% cholesterol. Also no significant differences were found in feed intake (FI) in all treatments. With dietary cholesterol increasing, a general upward trend of total cholesterol (TC), free cholesterol (FC), cholesterol ester (CE), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) in serum was exhibited. However, these kinds of cholesterol in serum were plateaued when fish fed diets with approximately over 1.30 to 1.80% cholesterol. The results of TC in liver and feces showed that, with increasing dietary cholesterol, only TC in feces exhibited an increasing trend. Quantitative PCR (qPCR) was used to assess the effects of dietary cholesterol on rate limiting enzyme 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase in cholesterol synthesis and cholesterol 7α-hydroxylase (CYP7A1) in bile acid synthesis. HMG-CoA reductase expression in liver was significantly suppressed with increasing dietary cholesterol, while CYP7A1 expression in liver was significantly enhanced as dietary cholesterol increased. There were no significant differences of ghrelin expression in both gut and brain. It can be concluded that moderate dietary cholesterol was beneficial to growth performance, while feed intake promotion effect was limited in juvenile turbot in the present study. Feedback control might exist in the cholesterol metabolism of turbot to keep cholesterol in homeostasis.

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