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The present study was conducted to determine the effect of waterborne copper (Cu) exposure on carnitine concentration, carnitine palmitoyltransferases I (CPT I) kinetics, and expression levels of four CPT I isoforms in the liver, muscle and heart of yellow catfish Pelteobagrus fulvidraco . Yellow catfish were exposed to four waterborne copper (Cu) concentrations (2 (control), 24 (low), 71 (medium), 198 (high) μg Cu/l, respectively) for 6 weeks. Waterborne Cu exposure increased maximal reaction rates (Vmax) in the liver and muscle, but not in the heart. Michaelis–Menten constants (Km) tended to increase in the liver, but decreased in the heart after Cu exposure. The contents of total carnitine (TC) and acylcarnitine (AC) in the liver, and free carnitine (FC) in the muscle increased with increasing waterborne Cu concentrations, while FC content in the muscle declined with the increase of Cu levels. Waterborne Cu exposure also significantly influenced carnitine composition and profiles in heart. The mRNA expression of CPT Iα1a, CPT Iα1b and CPT Iα2a in the liver, and CPT Iα1a, CPT Iα1b and CPT Iβ in the muscle as well as CPT Iα1a in the heart were up-regulated by Cu exposure. Additionally, correlations were observed in the expression levels of CPT I isoforms and Km for carnitine, and between CPT I isoform expression and CPT I activity. To our knowledge, for the first time, the present study provided evidence that waterborne Cu exposure could influence carnitine composition, CPT I kinetics and mRNA levels of four CPT I isoforms in yellow catfish, which served to increase our understanding of the mechanisms underlying lipid catabolism during Cu exposure. [ABSTRACT FROM AUTHOR]

The present study was conducted to determine the effect of dietary Cu deficiency and excess on carnitine status, kinetics and expression of CPT I in the liver and muscle of juvenile yellow catfish Pelteobagrus fulvidraco . To this end, yellow catfish were fed 0.76 (Cu deficiency), 4.18 (adequate Cu) and 92.45 (Cu excess) mg Cu kg − 1 diet, respectively, for 8 weeks. In the liver, Cu deficiency did not significantly affect the contents of FC, TC and AC, and the ratios of AC/FC and FC/TC. However, Cu excess reduced FC, TC and AC contents, and the ratio of AC/FC, but increased FC/TC ratio. In the muscle, dietary Cu levels showed no significant effects on the contents of FC, TC and AC as well as the ratio of FC/TC, but Cu excess significantly increased the ratio of AC/FC. Compared to the adequate Cu group, dietary Cu deficiency did not significantly affect the Vmax and Km values, and the ratio of Vmax/Km in the liver and muscle. However, Cu excess decreased Vmax and Vmax/Km ratio in the liver, and increased Vmax in the muscle. The mRNA expression of CPT Iα1a, CPT Iα1b, CPT Iα2a and CPT Iβ in the liver and muscle was influenced by dietary Cu levels. To our knowledge, the present study provided, for the first time, evidence that dietary Cu deficiency and excess differentially influenced carnitine status, kinetics and expression profiles of CPT I of yellow catfish, which would extend our understanding on Cu nutrition in fish. [ABSTRACT FROM AUTHOR]

Highlights: [•] Waterborne Zn exposure differentially affects carntine composition in fish. [•] Differential effect on CPT I kinetics is found in fish exposed to Zn. [•] Zn differentially affects the mRNA levels of four CPT I isoforms in fish. [•] Zn changes CPT I kinetics via altering its expression and carnitine status. [Copyright &y& Elsevier]

Abstract: The present study is conducted to determine the potential mechanisms of Zn on hepatic lipid deposition and metabolism for yellow catfish Pelteobagrus fulvidraco with 8-week chronic exposure to low Zn levels (Zn levels: 0.05, 0.35 and 0.86mg/l Zn, respectively) and 96-h acute exposure to a high Zn level (Zn level: 4.71mg/l Zn, respectively). For that purpose, hepatic lipid deposition and Zn accumulation, hepatic carnitine palmitoyltransferase I (CPT I) and lipoprotein lipase (LPL) activities, and the hepatic mRNA expression of ten genes involved in lipid metabolism are determined. Chronic (8 weeks) exposure to low Zn levels apparently increases hepatic lipid content, hepatosomatic index (HSI) (P <0.05) and LPL activity, and reduces hepatic CPT I activity. In contrast, the acute (96h) exposure to high Zn level reduces hepatic lipid content, HSI and LPL activity, and increases CPT I activity. The change of mRNA levels of genes related to lipid metabolism is Zn concentration-dependent. Pearson correlations among mRNA expression levels, lipid content, CPT I and LPL activities in liver are also observed in yellow catfish with the 8-week chronic Zn exposure. For the first time, our study demonstrates the effect of waterborne Zn exposure on lipid metabolism at the molecular levels in fish, which may contribute to understanding the mechanism of Zn-induced hepatic toxicity in fish. [Copyright &y& Elsevier]

The present study was conducted to determine the potential mechanisms of dietary Zn influencing lipid deposition in yellow catfish Pelteobagrus fulvidraco . For that purpose, yellow catfish were fed three diets containing different Zn levels including 19.82 (adequate Zn), 11.45 (Zn deficiency), 155.97 (Zn excess) mg Zn kg − 1 for 8 weeks, respectively. Lipid and Zn contents, CPT I and LPL activities, and mRNA expression of 12 genes involved in lipid metabolism in the liver and muscle, were determined. As compared to adequate Zn group, excessive dietary Zn apparently reduced lipid content in the liver and muscle, and LPL activity in the muscle, and increased activities of CPT I and LPL in the liver. Dietary Zn deficiency tended to enhance lipid accumulation and CPT I activity in both tissues. Dietary Zn excess increased Zn accumulation in the liver, muscle and whole fish, but dietary Zn deficiency reduced Zn content in the liver and whole fish. In the liver, dietary Zn deficiency significantly down-regulated the transcriptional levels of CPT 1A, PPARα, LepR, G6PD, 6PGD and ACCb, but up-regulated FAS mRNA levels. Dietary Zn excess up-regulated mRNA levels of CPT 1A, PPARα, Lep, LepR, SREBP-1, G6PD, 6PGD, ACCb and LPL, but down-regulated mRNA levels of FAS, ACCa and PPARγ. In the muscle, dietary Zn deficiency down-regulated mRNA levels of PPARα, Lep, SREBP-1, FAS and ACCa, and increased 6PGD and LPL gene expression. Dietary excess Zn down-regulated mRNA levels of PPARγ, SREBP-1, G6PD, ACCa, and LPL, and up-regulated mRNA levels of CPT 1A and Lep. For the first time, our study clearly indicated the different effects of dietary Zn deficiency and excess on lipid deposition and metabolism, which provided new insights into Zn nutrition and toxicology in fish. [ABSTRACT FROM AUTHOR]

Abstract: The present study was conducted to determine the effect of dietary Zn deficiency and excess on carnitine status, kinetics and expression of CPT I in the liver and muscle of yellow catfish Pelteobagrus fulvidraco. Yellow catfish were subjected to 20 (adequate Zn), 11.45 (Zn deficiency) and 155(Zn excess)mgkg−1 diet for 8weeks. In the liver, Zn deficiency increased FC, AC and TC contents and did not significantly affect the ratios of FC/TC and AC/FC. Similarly, Zn excess also increased TC and AC contents, and AC/FC ratios, but reduced FC content and FC/TC ratio. In the muscle, FC content was promoted by Zn deficiency and inhibited by Zn excess. FC/TC ratio was stimulated by Zn deficiency and inhibited by Zn excess. In contrast, AC/FC ratio was reduced by Zn deficiency and induced by Zn excess. Zn deficiency also reduced Km and Vmax values while Zn excess increased them in the liver and muscle. Zn deficiency and excess influenced the expression levels of four CPT I isoforms, such as CPT Iα1b, CPT Iβ, CPT Iα2a and CPT Iα1a in the liver and muscle. Furthermore, some correlations were observed in between the expression levels of CPT I isoforms and Km for carnitine, and between CPT I isoform expression and CPT I activity. Thus, for the first time, our study indicated that Zn deficiency and excess showed differential effects on carnitine status, kinetics and expression of CPT I in yellow catfish, which helped provide some novel insights into Zn nutrition and toxicology in fish. [Copyright &y& Elsevier]

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]