This study aimed to assess the effects of replacing fish meal with cottonseed meal protein hydrolysate (CPH) on the growth, intestinal function, growth hormone/insulin-like growth factor I (GH/IGF-I) axis, and inflammation of blunt snout bream, Megalobrama amblycephala. A total of 300 fish (38.66 ± 0.08 g) were allocated into five groups and fed either the basal diet (CPH 0) or the basal diet that replaced fish meal with 1% (CPH 1), 3% (CPH 3), 5% (CPH 5), and 7% CPH (CPH 7). Dietary CPH 3 increased the activities of protease, Na + /K +-ATPase, amylase, creatine kinase, and γ-glutamyl transpeptidase; microvillus length in the anterior and mid intestines; and the mRNA levels of GH, growth hormone receptor (GHR), and IGF-I without any negative effects on growth. Dietary CPH 7 increased the mRNA levels of tumor necrosis factor-α, interleukin-6, IκB kinase alpha, and nuclear factor κB but decreased the transcript level of inhibitor of κB-α (p < .05). Therefore, replacing fish meal with CPH 3 improved intestinal function and the transcription of GH/IGF-I axis genes without
This study was conducted to understand the effect of high‐fat diet challenge on lipid accumulation and inflammation in blunt snout bream. Fish (initial body weight: 41.84±0.07g) were fed a control diet or a high‐fat diet (HFD) for 9weeks, and the isolated primary hepatocytes were treated with 0.4mM oleic acid (OA) and/or 10ng/ml TNF‐α for 24hr. The results of the growth performance and feed utilization showed that short‐term feeding of HFD could increase energy intake and WGR, but long‐term feeding of HFD could inhibit feed intake. Hepatic steatosis and inflammation were observed in the HFD group according to enzyme activities or transcription levels of the related genes. In vitro, compared to untreated hepatocytes from fish fed a control diet, exposure of hepatocytes to OA could not only induce lipid accumulation but also promote pro‐inflammatory cytokines, such as TNF‐α and IL‐6. Increased fatty acid synthesis and decreased fatty acid oxidation were found in hepatocytes treated with TNF‐α alone, and co‐incubation of hepatocytes with OA and TNF‐α had a more substantial impact on lipid metabolism. Taken together, our results indicated that pro‐inflammatory cytokine TNF‐α was a crucial mediator of lipid accumulation in the liver of blunt snout bream fed HFD.
Six diets were designed to investigate the effects of dietary docosahexaenoic acid (22:6n‐3; DHA) levels (0.5, 1.3, 2.3, 4.2, 8.1 and 15.9 g/kg diets) on growth performance, fatty acid profile and expression of some lipogenesis‐related genes of blunt snout bream (Megalobrama amblycephala). Fish (average weight: 26.40 ± 0.11 g) were randomly fed one of six diets for 8 weeks. Results indicated that the final body weight (FBW) and specific growth rate (SGR) of fish fed 1.3 g/kg DHA were significantly higher than other groups except for the 2.3 g/kg DHA (p < .05). Compared with other groups, the number of lipid droplet clusters of the liver stained with oil red O in the 2.3 g/kg DHA group was the highest, which was consistent with the lipid contents of whole body and liver. The DHA proportion in liver and muscle significantly increased with the increasing dietary DHA levels (p < .05), which reflected fatty acid profiles of diets. The highest mRNA expressions of acetyl‐CoA carboxylase α (ACCα), fatty acid synthase (FAS) and sterol regulatory element‐binding protein‐1 (SREBP‐1) occurred in the 1.3 g/kg DHA group, followed by 2.3 g/kg DHA. In summary, the supplementation of 1.3–2.3 g/kg DHA could improve growth performance and lipogenesis, and the dietary DHA could improve DHA and PUFA proportion in liver and muscle.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.