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The aim of this article was to investigate the mechanism of appetite suppression induced by high-fat diets (HFD) in blunt snout bream (Megalobrama amblycephala). Fish (average initial weight 40·0 (sem 0·35) g) were fed diets with two fat levels (6 and 11 %) with four replicates. HFD feeding for 30 d could significantly increase the weight gain rate, but feeding for 60 d cannot. Food intake of M. amblycephala began to decline significantly in fish fed the HFD for 48 d. HFD feeding for 60 d significantly reduced the expression of neuropeptide Y and elevated the expression of cocaine- and amphetamine-regulated transcript (CART), actions both in favour of suppression of appetite. The activation of fatty acid sensing was partly responsible for the weakened appetite. In addition, inflammatory factors induced by the HFD may be involved in the regulation of appetite by increasing the secretion of leptin and then activating the mammalian target of rapamycin (mTOR). Lipopolysaccharide (LPS, 2·0 mg/kg of fish weight) was administered to induce inflammation, and sampling was performed after 3, 6, 9, 12, 18, 24 and 48 h of LPS injection. Within 6–24 h of LPS injection, the food intake and appetite of M. amblycephala decreased significantly, whereas the mRNA expression of leptin and mTOR increased significantly. Our results indicate that inflammatory cytokines may be the cause of appetite suppression in M. amblycephala fed a HFD.

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This research investigated the effects of dietary cholesterol (CHO) on growth, molting performance, CHO deposition, and lipid metabolism of Chinese mitten crab (Eriocheir sinensis). Six diets were formulated to contain 0% (control), 0.1%, 0.2%, 0.4%, 0.8%, and 1.6% CHO and were administered to E. sinensis 43.35 ± 0.05   g , for 16 weeks. From our results, crabs fed with 0.2% and 0.4% CHO diet, the final body weight (FBW), and weight gain ratio (WGR) increased significantly and the feed conversion ratio (FCR) decreased significantly compared with that of the control group. Furthermore, the molting performance of E. sinensis was significantly improved in crabs fed 0.2% CHO. Meanwhile, 0.2% CHO tends to upregulate molt-promoting genes and downregulate the expression of molt-inhibiting genes. It indicated that CHO might improve the molting performance of crabs by regulating ecdysteroid signal pathway transduction. In addition, dietary CHO can significantly increase the content of CHO in the hepatopancreas, muscle, and hemolymph. Moreover, dietary CHO increases the content of triglyceride (TG) in the hepatopancreas and hemolymph. The gene-related lipid metabolism shows that CHO may increase the lipid content by promoting lipid synthesis and inhibiting lipolysis. According to the results of this study, the dietary CHO requirement of E. sinensis is 0.27% for growth requirement and 0.45% for tissue CHO deposition based on the broken-line model.