Different effects of dietary Zn deficiency and excess on lipid metabolism in yellow catfish Pelteobagrus fulvidraco

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.