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This research was conducted to investigate the effects of four dietary zinc (Zn) sources on growth performance, Zn metabolism, antioxidant capacity, endoplasmic reticulum (ER) stress, and tight junctions in the intestine of grass carp Ctenopharyngodon idella. Four Zn sources consisted of Zn dioxide nanoparticles (ZnO NPs), Zn sulfate heptahydrate (ZnSO4·7H2O), Zn lactate (Zn-Lac), and Zn glycine chelate (Zn-Gly), respectively. Grass carp with an initial body weight of 3.54 g/fish were fed one of four experimental diets for 8 weeks. Compared to inorganic Zn (ZnSO4·7H2O), grass carp fed the ZnO NPs and Zn-Gly diets exhibited better growth performance. Furthermore, grass carp fed the organic Zn (Zn-Lac and Zn-Gly) diets displayed enhanced Zn transport activity, improved intestinal histology, and increased intestinal tight junction-related genes expression compared to other groups. In comparison to other Zn sources, dietary ZnO NPs caused increased Zn deposition and damaged antioxidation capacity by suppressing antioxidant enzymatic activities and related gene expression in the intestine. Grass cap fed the ZnO NPs diet also exhibited lower mRNA abundance of endoplasmic reticulum (ER) stress- and tight junction-associated genes. According to the above findings, it can be concluded that dietary organic Zn addition (Zn-Lac and Zn-Gly) is more beneficial for intestinal health in grass carp compared to inorganic and nanoform Zn sources. These findings provide valuable insights into the application of organic Zn sources, specifically Zn-Lac and Zn-Gly, in the diets for grass carp and potentially for other fish species. [ABSTRACT FROM AUTHOR]

Increasing dietary replacement levels of fish meal by alternative plant proteins are of value for aquaculture. Here, a 10-week feeding experiment was undertaken to explore the effects of fish meal replacement by mixed plant protein (at a 2 : 3 ratio of cottonseed meal to rapeseed meal) on growth performance, oxidative and inflammatory responses, and mTOR pathway of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (2.38 ± 0.1 g , mean ± SEM) were randomly divided into 15 indoors fiberglass tanks, 30 fish each tank, and fed five isonitrogenous (44% crude protein) and isolipidic (9% crude fat) diets with fish meal replaced by mixed plant protein at 0% (the control), 10% (RM10), 20% (RM20), 30% (RM30), and 40% (RM40), respectively. Among five groups, fish fed the control, and RM10 diets tended to have higher growth performance, higher protein content, and lower lipid content in livers. Dietary mixed plant protein substitute increased hepatic free gossypol content and damaged liver histology and reduced the serum total essential amino acids, total nonessential amino acids, and total amino acid contents. Yellow catfish fed the control, and RM10 diets tended to have higher antioxidant capacity. Dietary mixed plant protein replacement tended to promote proinflammatory responses and inhibited mTOR pathway. Based on the second regression analysis of SGR against mixed plant protein substitutes, the optimal replacement level of fish meal by mixed plant protein was 8.7%. [ABSTRACT FROM AUTHOR]

Currently, the effect of selenium and oxidized fish oil interactions on the intestinal lipid metabolism and antioxidant responses of fish remains unknown. Herein, yellow catfish Pelteobagrus fulvidraco (weight: 3.99 ± 0.01 g) were used as experimental animals and were fed four diets: an adequate amount of selenium (0.25 mg kg−1) with fresh fish oil (A-Se+FFO), an adequate amount of selenium with oxidized fish oil (A-Se+OFO), a high amount of selenium (0.50 mg kg−1) with fresh fish oil (H-Se+FFO), and a high amount of selenium with oxidized fish oil (H-Se+OFO). The feeding experiment was conducted for 10 weeks. The results showed that selenium supplementation alleviated the intestinal tissue damage and reduced the lipid accumulation that was induced by oxidized fish oils. Meanwhile, we also found that 0.50 mg kg−1 selenium reduced the oxidative stress that is caused by oxidized fish oils through increasing the GSH and the activity and mRNA expression of antioxidant enzymes. Dietary selenium and oxidized fish oils also affected the mRNA expression of intestinal selenoproteins including selenow2a, selenop2, and selenot2. Mechanistically, Se and oxidized eicosapentaenoic acid (oxEPA) influenced the GSH content by affecting the DNA binding ability of activating transcription factor (ATF) 3 to the slc7a11 promoter. For the first time, our results suggested that selenium alleviated the oxidized fish oil-induced intestinal lipid deposition and the oxidative stress of the fish. We also elucidated the novel mechanism of selenium increasing the GSH content by affecting the interaction of ATF3 and the slc7a11 promoter. [ABSTRACT FROM AUTHOR]

Zip family proteins are involved in the control of zinc (Zn) ion homeostasis. The present study cloned the promoters and investigated the transcription responses and protein subcellular localizations of three LIV-1 subfamily members (zip10, zip13, and zip14) from common freshwater teleost yellow catfish, Pelteobagrus fulvidraco, using in vitro cultured HEK293T model cells. The 2278 bp, 1917 bp, and 1989 bp sequences of zip10, zip13, and zip14 promoters, respectively, were subcloned into pGL3-Basic plasmid for promoter activity analysis. The pcDNA3.1 plasmid coding EGFP tagged pfZip10, pfZip13, and pfZip14 were generated for subsequent confocal microscope analysis. Several potential transcription factors' binding sites were predicted within the promoters. In vitro promoter analysis in the HEK293T cells showed that high Zn administration significantly reduced the transcriptional activities of the zip10, zip13, and zip14 promoters. The −2017 bp/−2004 bp MRE in the zip10 promoter, the −360 bp/−345 bp MRE in the zip13 promoter, and the −1457 bp/−1442 bp MRE in the zip14 promoter were functional loci that were involved in the regulation of the three zips. The −606 bp/−594 bp KLF4 binding site in the zip13 promoter was a functional locus responsible for zinc-responsive regulation of zip13. The −1383 bp/−1375 bp STAT3 binding site in the zip14 promoter was a functional locus responsible for zinc-responsive regulation of zip14. Moreover, confocal microscope analysis indicated that zinc incubation significantly reduced the fluorescence intensity of pfZip10-EGFP and pfZip14-EGFP but had no significant influence on pfZip13-EGFP fluorescence intensity. Further investigation found that pfZip10 localizes on cell membranes, pfZip14 colocalized with both cell membranes and lysosome, and pfZip13 colocalized with intracellular ER and Golgi. Our research illustrated the transcription regulation of zip10, zip13, and zip14 from P. fulvidraco under zinc administration, which provided a reference value for the mechanisms involved in Zip-family-mediated control of zinc homeostasis in vertebrates. [ABSTRACT FROM AUTHOR]

Dysregulation in hepatic lipid synthesis by excess dietary carbohydrate intake is often relevant with the occurrence of fatty liver; therefore, the thorough understanding of the regulation of lipid deposition and metabolism seems crucial to search for potential regulatory targets. In the present study, we examined TAG accumulation, lipid metabolism-related gene expression, the enzyme activities of lipogenesis-related enzymes, the protein levels of transcription factors or genes involving lipogenesis in the livers of yellow catfish fed five dietary carbohydrate sources, such as glucose, maize starch, sucrose, potato starch and dextrin, respectively. Generally speaking, compared with other carbohydrate sources, dietary glucose promoted TAG accumulation, up-regulated lipogenic enzyme activities and gene expressions, and down-regulated mRNA expression of genes involved in lipolysis and small ubiquitin-related modifier (SUMO) modification pathways. Further studies found that sterol regulatory element binding protein 1 (SREBP1), a key transcriptional factor relevant to lipogenic regulation, was modified by SUMO1. Mutational analyses found two important sites for SUMOylation modification (K254R and K264R) in SREBP1. Mutant SREBP lacking lysine 264 up-regulated the transactivation capacity on an SREBP-responsive promoter. Glucose reduced the SUMOylation level of SREBP1 and promoted the protein expression of SREBP1 and its target gene stearoyl-CoA desaturase 1 (SCD1), indicating that SUMOylation of SREBP1 mediated glucose-induced hepatic lipid metabolism. Our study elucidated the molecular mechanism of dietary glucose increasing hepatic lipid deposition and found that the SREBP-dependent transactivation was regulated by SUMO1 modification, which served as a new target for the transcriptional programmes governing lipid metabolism. [ABSTRACT FROM AUTHOR]

Disturbances in lipid metabolism are at the core of several health issues facing modern society, including fatty liver and obesity. The sterol regulatory element-binding protein 1 (SREBP-1) is one important transcription factor regulating lipid metabolism, but the relevant mechanism still remains unknown. The present study determined the transcriptional regulation of SREBP-1 and its target genes (including acetyl-CoA carboxylase α (accα), fatty acid synthase (fas) and stearoyl-CoA desaturase 1 (scd 1)) in a freshwater teleost, grass carp Ctenopharyngodon idella. We cloned and characterised the 1988 bp, 2043 bp, 1632 bp and 1889 bp sequences of srebp -1, accα , scd 1 and fas promoters, respectively. A cluster of putative binding sites of transcription factors, such as specific protein, yin yang 1, nuclear factor Y, sterol response elements (SRE) and enhancer box (E-box) element, were predicted on their promoter regions. Overexpression of nSREBP-1 reduced srebp -1 promoter activity, increased scd 1 and fas promoter activity but did not influence accα promoter activity. The site-mutation and electrophoretic mobility shift assay analysis indicated that srebp- 1 , fas and scd 1 promoters, but not accα promoter, possessed SRE. In Ctenopharyngodon idella kidney (CIK) cells of grass carp, nSREBP-1 overexpression significantly reduced srebp -1 mRNA expression and up-regulated miR-29 mRNA expression. The 3′UTR of srebp- 1 possessed the potential miR-29 binding site and miR-29 up-regulated the luciferase activity of srebp- 1 3′UTR and srebp -1 mRNA expression, implying a self-activating loop of SREBP-1 and miR-29 in grass carp. Based on the above-mentioned results, we found two novel transcriptional mechanisms for SREBP-1 in grass carp: (1) the auto-regulation sited on the SREBP-1 promoter regions was suppressive and (2) there was a self-activating loop of SREBP-1 and miR-29. [ABSTRACT FROM AUTHOR]

SUMOylation is a kind of important post-translational modification. In the present study, we identified 10 key genes involved in SUMOylation and deSUMOylation (sumo1, sumo2, sumo3, sae1, uba2, ubc9, pias1, senp1, senp2 , and senp3) in yellow catfish Pelteobagrus fulvidraco , investigated their tissue expression patterns and transcriptional responses to carbohydrate addition both in vivo and in vitro. All of these members shared similar domains to their orthologous genes of other vertebrates. Their mRNAs were widely expressed in all the tested tissues, but at variable levels. Dietary carbohydrate levels differentially influenced the mRNA levels of these genes in liver, muscle, testis, and ovary of yellow catfish. Their mRNA levels in primary hepatocytes were differentially responsive to glucose addition. Our study would contribute to our understanding into the molecular basis of SUMOylation modification and into the potential SUMOylation function in the carbohydrate utilization in fish. [ABSTRACT FROM AUTHOR]

Peroxisome proliferator-activated receptor beta (PPARβ) is a ligand-activated transcription factor that plays critical roles in the regulation of many important physiological processes. In this study, PPARβ was cloned and characterized in yellow catfish Pelteobagrus fulvidraco. PPARβ cDNA was 2350 bp in length with an open reading frame (ORF) of 1530 bp, encoding 509 amino acids, a 5′-untranslated region (UTR) of 474 bp, and a 3′-UTR of 346 bp. Similar to mammals, PPARβ protein was predicted to consist of four domains, the A/B domain, DNA-binding domain (DBD), D domain, and ligand-binding domain (LBD). The DBD contained two zinc fingers with eight conserved cysteine residues. The predicted secondary structure of LBD consisted of 12 highly conserved α-helices and a small β-sheet of 4 strands. In addition, PPARβ was widely expressed across the tested tissues (liver, heart, muscle, intestine, brain, spleen, kidney, fat, ovary, and gill), but at the variable levels. Furthermore, the transcriptional responses of PPARβ by dietary Cu and Zn levels were also investigated. Dietary Cu levels showed no significant effects on PPARβ mRNA levels in the liver and intestine; in contrast, dietary Zn levels upregulated the hepatic PPARβ mRNA levels, but not in the intestine. The present study serves to increase our understanding into the function of the PPARβ gene in fish. [ABSTRACT FROM AUTHOR]

Janus kinase (JAK) is a family of non-receptor tyrosine kinases that participate in transducing cytokine signals from the external environment to the nucleus in various biological processes. Currently, information about their genes structure and evolutionary history has been extensively studied in mammals as well as in several fish species. By contrast, limited reports have addressed potential role of diverse JAK in signaling responses to leptin in fish. In this study, we identified and characterized five JAK members of Synechogobius hasta . Compared to mammals, more members of the JAK family were found in S. hasta , which provided evidence that the JAK family members had arisen by the whole genome duplications during vertebrate evolution. For protein structure, all of these members possessed similar domains compared with those of mammals. Their mRNAs were expressed in a wide range of tissues, but at the different levels. Incubation in vitro of freshly isolated hepatocytes of S. hasta with different concentrations of recombinant human leptin decreased the intracellular triglyceride content and lipogenic genes expression, and increased mRNA expression of several JAK and lipolytic genes. AG490, a specific inhibitor of JAK, reversed leptin-induced effects on TG content and JAK2a, JAK2b, hormone-sensitive lipase (HSL2) and acetyl-CoA carboxylase (ACCa), indicating that the JAK2a/b may have mediated the actions of leptin on lipid metabolism at transcriptional level. [ABSTRACT FROM AUTHOR]

Comprehensive knowledge of osteological development of fish not only provides means for understanding its functional development, but also allows early detection of skeletal anomalies. The present study was conducted to determine osteological development and occurrence of anomalies from the first to the 40th day after hatching ( DAH) for yellow catfish Pelteobagrus fulvidraco, a commercially important species in China. Vertebral ontogeny started with formation of anterior neural arches at 3 DAH, and completed at 6 DAH. Vertebral centra started to develop at 4 DAH and ossification in all centra was visible at 15 DAH. Caudal fin appeared at 2 DAH and ossification was visible at 26 DAH. The onset of dorsal and anal fins appeared at 4 DAH and their ossifications were visible at 20 DAH. Pectoral fins were present before first feeding and formed entirely at 9 DAH, and their ossifications were visible at 21 DAH. Pelvic fins appeared at 9 DAH, and formed completely at 21 DAH. The ossification of pelvic fins was not finished until the end of the experiment (40 DAH). 24 types of skeletal anomalies were observed. About 20% of individuals showed at least one anomaly. Haemal vertebrae anomalies occurred at the highest frequency, followed by pre-haemal, caudal vertebrae and anal fin anomalies, and caudal fin had the lowest anomalies frequency. For the first time, our study determined osteological development and anomalies incidence in larval yellow catfish, which help further investigations into rearing conditions leading to appearance of these anomalies to prevent their incidence. [ABSTRACT FROM AUTHOR]

The present study clones and characterizes the full-length cDNA sequences of members in JAK–STAT pathway, explores their mRNA tissue expression and the biological role in leptin influencing lipid metabolism in yellow catfish Pelteobagrus fulvidraco . Full-length cDNA sequences of five JAKs and seven STAT members, including some splicing variants, were obtained from yellow catfish. Compared to mammals, more members of the JAKs and STATs family were found in yellow catfish, which provided evidence that the JAK and STAT family members had arisen by the whole genome duplications during vertebrate evolution. All of these members were widely expressed across the eleven tissues (liver, white muscle, spleen, brain, gill, mesenteric fat, anterior intestine, heart, mid-kidney, testis and ovary) but at the variable levels. Intraperitoneal injection in vivo and incubation in vitro of recombinant human leptin changed triglyceride content and mRNA expression of several JAKs and STATs members, and genes involved in lipid metabolism. AG490, a specific inhibitor of JAK2–STAT pathway, partially reversed leptin-induced effects, indicating that the JAK2a/b–STAT3 pathway exerts main regulating actions of leptin on lipid metabolism at transcriptional level. Meanwhile, the different splicing variants were differentially regulated by leptin incubation. Thus, our data suggest that leptin activated the JAK/STAT pathway and increases the expression of target genes, which partially accounts for the leptin-induced changes in lipid metabolism in yellow catfish. [ABSTRACT FROM AUTHOR]

Lipid overload-induced hepatic cholesterol accumulation is a major public health problem worldwide, and choline has been reported to ameliorate cholesterol accumulation, but its mechanism remains unclear. Our study found that choline prevented high-fat diet (HFD)-induced cholesterol metabolism disorder and enhanced choline uptake and phosphatidylcholine synthesis in the liver tissues; choline incubation prevented fatty acid (FA)-induced cholesterol accumulation and FA-induced inhibition of bile acid synthesis. Moreover, compared to single FA incubation, choline incubation or FA + choline co-incubation increased the mRNA abundances and protein levels of HNF4α and up-regulated the degradation of cholesterol into bile acids. Mechanistically, choline prevented the FA-induced accumulation of SREBP2 protein and the interaction between SREBP2 and HNF4α, thereby enhancing the DNA binding capacity of the HNF4α to the CYP7A1 promoter, and promoting the degradation of cholesterol into bile acids. Our study elucidated the novel regulatory mechanisms of choline preventing HFD-induced cholesterol accumulation and increasing bile acid synthesis by SREBP-2/HNF-4α/CYP7A1 pathway. • Choline prevented high-fat diet-induced cholesterol metabolism disorder. • Choline prevented FA-induced cholesterol accumulation and inhibition of bile acid synthesis. • Choline increased HNF4α expression and up-regulated cholesterol degradation. • Choline prevented the FA-induced interaction between SREBP2 and HNF4α. • Choline enhanced HNF4α binding capacity to CYP7A1 promoter, and promoted cholesterol degradation. [ABSTRACT FROM AUTHOR]

The present study was conducted to determine the effect of leptin on lipid metabolism in ovarian follicle cells of yellow catfish Pelteobagrus fulvidraco . For that purpose, primary ovarian follicle cells were isolated from yellow catfish, cultured and subjected to different treatments (control, 0.1% DMSO, 500 ng/ml leptin, 500 ng/ml leptin plus 100 μM wortmannin, 500 ng/ml leptin plus 50 nM AG490, respectively) for 48 h. Intracellular triglyceride (TG) content, the activities (CPT I, FAS, G6PD, and 6PGD) and/or expression level of several enzymes (CPT I, FAS, G6PD, 6PGD, ACCa and ACCb), as well as the mRNA expression of transcription factors (PPARα, PPARγ and SREBP-1) involved in lipid metabolism were determined. Recombinant human leptin (rt-hLEP) incubation significantly reduced intracellular TG content, activities and mRNA levels of FAS, G6PD and 6PGD, SREBP-1 and PPARγ, but enhanced activity and mRNA level of CPT I, PPARα and ACCa. Specific inhibitors AG490 and wortmannin of JAK–STAT and IRS–PI3K signaling pathways prevented leptin-induced changes, indicating that JAK–STAT and IRS–PI3K signaling pathways were involved in the process of leptin-induced changes of lipid metabolism. Based on these observations above, for the first time, our study indicated that leptin reduced lipid deposition by activating lipolysis and suppressing lipogenesis in ovarian follicles of yellow catfish, and both JAK–STAT and IRS–PI3K signaling pathways were involved in the changes of leptin-induced lipid metabolism. [ABSTRACT FROM AUTHOR]

This study was conducted to determine the ontogenetic development of the digestive tract and its accessory structures (liver, pancreas, and gall bladder) in agastric larval Chinese sucker Myxocyprinus asiaticus with the histological and ultrastructural approaches from hatching to 56 days after hatching ( DAH). On the basis of its feeding mode, and analyzing the main histological features of the digestive system, larval development in Chinese sucker was divided into three stages from hatching: stage 1 (endotrophic period): 1-6 DAH; stage 2 (endoexotrophic period): 7-14 DAH; stage 3 (exclusively exotrophic period): from 15 DAH onward. At hatching, the digestive tract of the larvae consisted of an undifferentiated straight tube. At 4 DAH, the mouth opened, and the digestive tract was differentiated into buccopharyngeal cavity, esophagus and intestine. At 7 DAH, fish started to feed exogenously. Yolk sac was completely exhausted at 15 DAH. Until 56 DAH, the digestive tract of the larvae displayed regularly arranged microvilli, abundant vacuoles, and protein inclusion bodies. The pancreas, liver, and gall bladder were functional from 6 DAH, which enabled larvae to ingest, digest, and assimilate the first exogenous food. In comparison with teleosts that have a stomach, the development of the digestive tract of the agastric Chinese sucker seemed relatively slow. [ABSTRACT FROM AUTHOR]

trans-10, cis-12 (t10c12) Conjugated linoleic acid (CLA) reduced body lipid deposition in various experimental animals, but the mechanisms involved were still emerging. Carnitine palmitoyltransferase I (CPT I) catalyzes an important regulatory step in lipid metabolism. At present, no studies, to our knowledge, have evaluated the kinetic constants influenced by dietary CLA in fish. In the present study, we tested the hypothesis that changes in body lipid content in fish as a response to dietary t10c12 CLA was related to the change of CPT I kinetic constants [Michaelis constant ( K), maximal velocity and catalytic efficiency for carnitine and palmitoyl-CoA]. Juvenile Synechogobius hasta were fed three experimental diets with fish oil replaced with 0 (control), 1, or 2 % t10c12 CLA for 8 weeks. Weight gain, specific growth rate and protein efficiency rate increased with dietary t10c12 CLA level. Dietary t10c12 CLA addition significantly reduced lipid contents both in liver and muscle. Dietary CLA addition also improved CPT I activities in muscle but did not significantly influence hepatic CPT I activity. CPT I kinetic parameters ( K, V and catalytic efficiency) were significantly influenced by t10c12 CLA. CPT I catalytic efficiencies with carnitine and palmitoyl-CoA as substrates were higher in muscle and liver of fish fed increasing t10c12 CLA. For the first time, the findings demonstrated effect of dietary CLA addition on CPT I kinetics in fish and supported our starting hypothesis that dietary t10c12 CLA addition induced alterations in CPT I kinetic constants of muscle and liver. Increased CPT I catalytic efficiency might be the main reason for reduced lipid deposition in these tissues by dietary t10c12 CLA supplementation. [ABSTRACT FROM AUTHOR]

An 8-week feeding trial was conducted to determine the effect of dietary conjugated linoleic acid ( CLA) on growth performance, muscle fatty acid profile, hepatic intermediary metabolism and antioxidant responses in genetically improved farmed Tilapia ( GIFT) strain of O reochromis niloticus (initial body weight: 42.6 ± 0.4 g, mean ± standard deviation). Three replicated groups of GIFT strain of Nile tilapia were hand-fed to satiation, twice a day, with the diets in which CLA oil, containing mainly the bioactive cis-9, trans-11 and trans-10, cis-12 isomers, was included at 0 (control), 0.5%, 1%, 1.5%, 2% and 2.5%, respectively, at the expense of fish oil to maintain the constant lipid and energy levels. Growth performance and feed utilization showed no significant differences among the treatments ( P > 0.05). The dietary inclusion of CLA modified total percentages of the main groups of fatty acids. Increasing saturated fatty acid content and reduced mono-unsaturated fatty acid contents in muscle were observed with increasing dietary CLA inclusion ( P < 0.05). Total n-3 fatty acids and total polyunsaturated fatty acids tended to decline with increasing dietary CLA levels ( P < 0.05), but n-6 fatty acids showed no significant differences among the treatments ( P > 0.05). Dietary CLA supplementation resulted in the significant increase in the trans-10, cis-12 and cis-9, trans-11 CLA isomers in muscle ( P < 0.05) and also significantly influenced several hepatic enzymatic activities, such as succinate dehydrogenase, lactate dehydrogenase, malic dehydrogenase, lipoprotein lipase and hepatic lipase activities ( P < 0.05). Reduced superoxide dismutase and glutathione peroxidase activities, and the decline in malondialdehyde levels were observed in fish fed the CLA-supplemented diets ( P < 0.05), indicating that dietary CLA supplementation showed a powerful antioxidant effect for this fish species. Our study was the first report involved in the effect of dietary CLA inclusion on hepatic intermediary metabolism and antioxidant responses in fish, which could be used as indicators of nutritional and physiological status of the fish species. [ABSTRACT FROM AUTHOR]

Abstract: The present study was conducted to determine dietary manganese (Mn) requirement for juvenile yellow catfish Pelteobagrus fulvidraco and evaluate the effect of dietary Mn levels on growth performance, whole body mineral composition and hepatic intermediary metabolism for this fish species. The six experimental diets were formulated to contain the graded levels of MnSO4·H2O (0, 3, 6, 12, 24 and 48mg Mn kg−1 diet, respectively), providing the actual dietary Mn values of 3.1 (control), 4.2, 5.3, 6.9, 12.0 and 19.5mg kg−1 diet, respectively. Each diet was assigned to three replicate groups of yellow catfish (initial body weight: 4.00±0.08, means±SD) for 8weeks. Percent weight gain (WG) increased with increasing dietary Mn levels from 3.1 to 5.3mgkg−1 diet and then plateaued above these levels. The lowest protein efficiency ratio (PER), and the highest feed conversion rate (FCR) were observed in fish fed the control diet and showed no significant differences among the other treatments. Dietary Mn supplementation did not significantly influence moisture, protein and ash contents in whole body, but whole body lipid content was the lowest for fish fed the 12.0 and 19.5mg Mn kg−1 diets. Condition factor and hepatosomatic index were observed to be the highest for fish fed the control diet. For whole body mineral composition, increasing Mn content, and declining calcium, phosphorus and iron contents were observed in fish fed the diets containing increasing Mn levels. For hepatic enzymatic activities, the Mn-SOD activities were observed to be the highest in fish fed the diets containing 5.3 and 6.9mg Mn kg−1, and the lowest for fish fed the control diet. Lactate dehydrogenase activity declined with increasing dietary Mn level from 3.1 to 5.3mg kg−1 diet, and then increased with dietary Mn level from 5.3 to 19.5mg kg−1 diet. Hepatic lipase activity was observed to be the highest for fish fed the diet containing 12.0mg Mn kg−1 and showed no significant differences among the treatments. Succinate dehydrogenase, malic dehydrogenase and lipoprotein lipase activities showed no significant differences among the treatments (P >0.05). Analysis by the broken-line regression of WG, PER and hepatic Mn-SOD activity indicated that the optimal dietary Mn requirements in juvenile yellow catfish were 5.5, 5.6 and 6.4mg kg−1 diet, respectively. [Copyright &y& Elsevier]

An 8-week experiment was conducted to examine the effect of partial replacement of fish meal (FM) by a mixture of soybean meal (SBM) and rapeseed meal (RM) in practical diets of juvenile Chinese mitten crab Eriocheir sinensis of initial body weight of 1.54±0.12 g (means±SD, n=90). Five isonitrogenous diets were formulated to contain 35% protein and 5% lipid. Soybean meal and RM mix (1:1 ratio) were included at five levels of 0 (control), 15%, 30%, 45% and 60%, replacing 0, 20%, 40%, 60% and 80% FM respectively. When FM was replaced by 15% of SBM and RM, crab showed the highest growth, feed utilization and moulting frequency (MF). Fish meal replaced by SBM and RM did not significantly influence crude protein, lipid and moisture contents of whole body crab, but ash content was the lowest for crab fed the diet with FM replaced by 15% of SBM and RM. Apparent digestibility coefficients (ADCs) of dry matter, crude protein and energy tended to decline with increasing inclusion levels of dietary SBM and RM. In general, ADCs of lipid were high (over 90%) and showed no significant differences among the treatments ( P>0.05). Based on these observations above, these results indicated that about 40% of FM can be replaced with a mixture of SBM and RM (1:1 ratio) in the diet of E. sinensis without adverse growth performance, compared with the FM-based diet. However, 20% of FM replaced by SBM and RM produced the best growth performance and feed utilization. [ABSTRACT FROM AUTHOR]

Abstract: The present study was conducted to determine dietary zinc (Zn) requirement for juvenile yellow catfish Pelteobagrus fulvidraco and evaluate the effect of dietary Zn levels on growth performance, whole body mineral composition, hepatic intermediary metabolism and antioxidant responses for this fish species. The six experimental diets were formulated to contain the graded levels of ZnSO4·7H2O (0, 0.002, 0.004, 0.008, 0.016 and 0.032%, respectively), providing the actual dietary Zn values of 7.60 (control), 11.90, 16.24, 24.81, 38.75 and 76.36mgkg−1 diet, respectively. Each diet was assigned to three replicate groups of yellow catfish (initial body weight: 6.08±0.12, means±SD) for 8weeks. Increasing dietary Zn level up to 16.24mgkg−1 diet increased growth performance and feed utilization, beyond which they remained nearly unchanged. Whole body lipid contents significantly declined, but whole body moisture and protein contents showed no significant differences with increasing dietary Zn levels. Whole body Zn content tended to increase with increasing dietary Zn level, whereas whole body Cu and Fe contents declined with dietary Zn addition. Hepatic succinate dehydrogenase (SDH), lactate dehydrogenase (LDH) and malic dehydrogenase (MDH) activities showed no significant differences among the treatments. However, lipoprotein lipase (LPL) and hepatic lipase (HL) activities increased with increasing dietary Zn levels. Superoxide dismutase (SOD) activity increased and malondialdehyde (MDA) level declined with increasing dietary Zn levels up to the requirement level. Hepatic catalase (CAT) activity showed no significant differences among the treatments. Analysis by the broken-line regression of specific growth rate (SGR) and protein efficiency rate (PER) indicated that dietary Zn requirements in juvenile yellow catfish were 17.12–20.86mgkg−1 diet. [Copyright &y& Elsevier]

The article investigates the developmental situation of the competitive sport in China's middle schools. Existing problems that were identified include inequality between sport and education in the combination of the two, lower level of coaches' teaching and training, and the continuing existence of the contradiction of learning and training.