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An 8-week feeding trial was conducted to evaluate the effects of dietary n-3 LC-PUFA levels on growth performance, tissue fatty acid profiles and relative expression of genes involved in the lipid metabolism of mud crab (Scylla paramamosain). Ten isonitrogenous diets were formulated to contain five n-3 LC-PUFA levels at 7 and 12 % dietary lipid levels. The highest weight gain and specific growth rate were observed in crabs fed the diets with 19·8 and 13·2 mg/g n-3 LC-PUFA at 7 and 12 % lipid, respectively. Moisture and lipid contents in hepatopancreas and muscle were significantly influenced by dietary n-3 LC-PUFA at the two lipid levels. The DHA, EPA, n-3 LC-PUFA contents and n-3:n-6 PUFA ratio in hepatopancreas and muscle significantly increased as dietary n-3 LC-PUFA levels increased at both lipid levels. The expression levels of -6 fatty acyl desaturase and acyl-CoA oxidase in hepatopancreas increased significantly, and expression levels of fatty acid synthase, carnitine palmitoyltransferase I and hormone-sensitive TAG lipase were down-regulated, with increased dietary n-3 LC-PUFA regardless of lipid level. Based on weight gain, n-3 LC-PUFA requirements of S. paramamosain were estimated to be 20·1 and 12·7 mg/g of diet at 7 and 12 % dietary lipid, respectively. Overall, dietary lipid level influenced lipid metabolism, and purified, high-lipid diets rich in palmitic acid reduced the n-3 LC-PUFA requirement of juvenile mud crab.

An 8-week feeding trail was conducted in Acanthopagrus schlegelii with an initial body weight of 8.34 ± 0.01g. Three isonitrogenous diets were formulated, (1) Control: medium-fat diet (12%); (2) HFD: high-fat diet (18%); (3) HFD + FF: high-fat diet with fenofibrate (0.15%). Liver histological analysis revealed that, compared to HFD, vacuolar fat drops were smaller and fewer in fish fed fenofibrate. Expression of lipid catabolism regulator peroxisome proliferator-activated receptor alpha (pparα) was up-regulated by fenofibrate compared with HFD. In addition, fenofibrate significantly increased the expression level of silent information regulator 1 (sirt1). Meanwhile, the expression level of anti-inflammatory cytokine interleukin 10 (il-10) in intestine was up-regulated, while pro-inflammatory cytokine interleukin 1β (il-1β) in liver and intestine were down-regulated by dietary fenofibrate supplementation. Overall, the present study indicated that fenofibrate reduced fat deposition and attenuated inflammation response caused by HFD partly through a pathway involving regulation of pparα and sirt1., Competing Interests: Declaration of competing interest The authors have declared that no competing interests exist., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The eggshell color of avian species is an important trait that is predominantly determined by the pigments biliverdin and protoporphyrin. Various factors affect eggshell pigment deposition and coloration; however, the underlying mechanisms remain unclear. We analyzed the hepatic transcriptomes and metabolomes of Changshun green-shell hens laying dark green and light green eggs to investigate the potential role of the liver in regulating the intensity of the green eggshell color. In total, 350 differentially expressed genes and 211 differentially altered metabolites were identified. Gene set enrichment analysis revealed that the enriched pathways and Gene Ontology (GO) terms were mainly associated with energy, immunity, and nutrient metabolism. Metabolite set enrichment analysis revealed that the enriched pathways were mainly associated with amino acid, vitamin, bile acid, and lipid metabolism. Moreover, gene–metabolite interaction network analysis revealed 1 subnetwork. Most genes and metabolites in this subnetwork were determined to be related to melanin metabolism and transport. In conclusion, our results suggest that hepatic melanin metabolism and transport are critical for eggshell coloration. Six candidate genes (CDKN2B, DDC, PYCR1, ABCG5, SLC3A1 , and P2RX2) and 7 candidate metabolites (serotonin, 5-hydroxyindoleacetic acid, ornithine, acetylcholine, L -tryptophan, D -ornithine, and ADP) were suggested to play important roles in this process. Meanwhile, this study suggests that changes in hepatic energy metabolism, immune status, antioxidation activity, nutrient availability, and bile acid synthesis can impair eggshell coloration. [ABSTRACT FROM AUTHOR]

The present study aimed to evaluate the effects of dietary inositol level (0.86, 1.34, 1.40, 2.30, 3.88 and 7.50 g kg−1) on glucose and lipid homeostasis in Litopenaeus vannamei. The results indicated that the contents of inositol, phosphatidyl inositol (PI) and glycogen in hepatopancreas and muscle, very low-density lipoprotein (VLDL) in hepatopancreas and hemolymph, the activity of carnitine palmitoyl-transferase (CPT1) and the expression of hmit and inox were positively related to the dietary inositol levels, while the contents of glucose (GLU), crustacean hyperglycemic hormone (CHH), triglyceride (TG), cholesterol (CHO) and non-esterified fatty acid (NEFA) in hemolymph and the expression of imp , pepck , g6pc and fbp were negatively correlated with the dietary inositol level. TG content, phosphoenolpyruvate carboxykinase (PEPCK) activity and the expression levels of srebp , fa s, acc1 , g6pd and 6gpd in shrimp fed 3.88 and 7.50 g kg−1 inositol diets were significantly lower compared with shrimp fed the basal diet, while the expression of cpt1 , aco , fabp , fatp and idir were showed the reverse change trend (P < 0.05). The activities of hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK) and the expression levels of ir, irs1 , pi3k and akt were significantly increased as dietary inositol levels ranged from 1.40 to 7.50 g kg−1, while the expression levels of gsk-3β and foxo1 significantly down-regulated. Hepatopancreas R cells number in shrimp fed 2.30, 3.88 and 7.50 g kg−1 inositol diets were significantly increased compared with shrimp fed 0.86 g kg−1 inositol diet, while the diameters and areas showed an opposite trend. In addition, dietary inositol supplementation significantly increased hemolymph insulin like peptide (ILP) content but had no significant effect on high density lipoprotein cholesterol (HLD C) content in hemolymph, hepatic lipase (HL) activity and the ratio of n-3/ n-6 PUFA and DHA/EPA in hepatopancreas. In conclusion, appropriate dietary inositol could positively regulate the Insulin-PI3K-Akt pathway to promote glucose utilization and maintain the normal accumulation of glycogen and lipids required for development, while high dietary inositol could promote lipid mobilization and prevent hepatopancreas lipids deposition by negatively regulating the Insulin-PI3K-Akt pathway, improving ILP sensitivity and enhancing VLDL synthesis, which may therefore be an important mechanism in the action of inositol on glucose and lipid metabolism. These findings provided further insight and understanding of mechanisms by which dietary inositol regulated glucose and lipid metabolism in L. vannamei. Possible pathways by which appropriate inositol level (blue line) and high inositol level (red line) regulation of glucose and lipid metabolism in L. vannamei. The line ends with arrows indicating facilitation, and the line ends with horizontal lines indicating inhibition. The black arrow indicates the path direction. Upward arrows represent up-regulation and downward arrows represent down-regulation. Ino, inositol; H-Ino, high level inositol level. PI, phosphatidylinositol; ILP, insulin like peptide; Glu, glucose; MIOX, myo-inositol oxygenase; IMP, inositol monophosphatase. [Display omitted] • Dietary inositol level affected the deposition of inositol and PI in tissues. • Dietary appropriate inositol promoted the development of hepatopancreas R cells. • Dietary appropriate inositol positively regulated the Insulin-PI3K-Akt pathway. • Optimal inositol in diet promote glucose utilization and moderate lipid accumulation. [ABSTRACT FROM AUTHOR]

An eight-week feeding trial was conducted to evaluate the influence of an alternating linseed oil (LO) and fish oil (FO) feeding strategy in black seabream A. schlegelii (initial weight, 8.49 ± 0.01 g). Two isonitrogenous and isolipidic feeds were formulated to contain FO or LO, and used to enable three feeding strategy treatments termed FO (feeding the FO diet for 8 weeks), LO (feeding the LO diet for 8 weeks) and FO re-feeding (feeding LO for 4 weeks then FO for 4 weeks). Fish in the FO re-feeding and FO groups had significantly higher final body weights (FBW), weight gains (WG), specific growth rates (SGR) but lower muscle lipid content than fish in the LO group. In muscle, the FO re-feeding strategy restored eicosapentaenoic and docosahexaenoic acid contents to 82.67% and 83.84%, respectively, of those in fish fed the FO treatment. In addition, the FO re-feeding strategy significantly down-regulated the expression levels of genes related to long-chain polyunsaturated fatty acid (LC-PUFA) biosynthesis and lipogenesis, including fatty acyl desaturase (fads2), elongase of very long-chain fatty acids 4a (elovl4a) and sterol regulatory element-binding protein-1 (srebp-1) compared to fish fed the LO treatment. Similarly, the hepatic Srebp-1c concentration in fish in the FO re-feeding group was markedly lower than in fish in the LO treatment group. Expression of the lipid catabolism gene adipose triglyceride lipase (atgl) was up-regulated in fish in the FO re-feeding group compared with fish in the LO group. Overall, the present study indicated that a strategy of re-feeding FO following feeding LO for four-week promoted growth, mitigated lipid accumulation in muscle, and effectively restored muscle n-3 LC-PUFA levels in A. schlegelii. • Dietary LO had an adverse effect on growth in A. schlegelii. • Growth and feed utilization were recovered by FO re-feeding in A. schlegelii. • FO re-feeding could effectively restore DHA and EPA contents in muscle. • After FO re-feeding, DHA and EPA were better retained in muscle than in liver. • FO-refeeding reduced lipid accumulation by regulating gene expression. [ABSTRACT FROM AUTHOR]