Differential effects of acute and chronic zinc (Zn) exposure on hepatic lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco

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 0.86 mg/l Zn, respectively) and 96-h acute exposure to a high Zn level (Zn level: 4.71 mg/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 (96 h) 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.

► Acute Zn exposure induces lipid depletion, mainly via up-regulated lipolysis and reduced import of lipids into liver.
► Chronic Zn exposure induces lipid accumulation through the inhibition of lipolysis and the improvement of lipogenesis.
► Our study determines the mechanism of waterborne Zn exposure on lipid metabolism in fish on a molecular level.
► Our study indicates the differential effect of acute and chronic Zn exposure on lipid deposition and metabolism in fish.