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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 © 2013 Elsevier B.V. All rights reserved.)

The present study was conducted to determine hepatic lipid metabolism and metal-element composition in Synechogobius hasta exposed to waterborne chronic copper (Cu) concentrations of control, 57, and 118 μg Cu/l, respectively, for 30 days. Growth decreased, but hepatosomatic index, viscerosomatic index, and hepatic lipid content increased with increasing waterborne Cu levels. Staining with oil red O showed extensive steatosis in liver of Cu-exposed fish. Cu exposure increased hepatic 6-phosphogluconate dehydrogenase, glucose-6-phosphate dehydrogenase, and malic enzyme activities, whereas fatty acid synthetase, isocitrate dehydrogenase, and carnitine palmitoyltransferases I activities remained unaffected. Cu, zinc, iron, and manganese contents were also changed in several tissues (gill, liver, spleen, gastrointestinal tract, and muscle) in a tissue-, dose-, and time-dependent manner. This was the first study to examine the effects of waterborne Cu exposure on several enzymatic activities mediating hepatic lipogenesis and lipolysis in fish as well as to show that waterborne Cu exposure could enhance the metabolism of lipid synthesis and consequently induce the increase of hepatic lipid deposition in S. hasta.

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]

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]