Effects of dietary Zn level on growth performance, lipolysis and expression of genes involved in the Ca2+/CaMKKβ/AMPK pathway in juvenile Pacific white shrimp.

The present study evaluated the effects of dietary zinc level on growth performance, serum and hepatopancreas metabolites, and expression of genes involved in lipid and energy metabolism, and the signal pathway of dietary Zn-induced lipolysis. Five isonitrogenous and isolipidic diets were formulated to contain different zinc levels: 46.4 (basal diet), 77.2, 87.0, 117.1, and 136.8 mg kg-1, respectively. The results indicated that shrimp fed the diet containing zinc at 117.1 mg kg-1 had higher weight gain and specific growth rate, and the lowest feed intake and feed conversion rate, than shrimp fed the other diets. The deposition rate of Zn in whole body significantly decreased with increasing dietary zinc level. Dietary Zn prevented the accumulation of free radicals and improved antioxidant activities by increasing Cu/Zn superoxide dismutase and reducing malonaldehyde in hepatopancreas. Dietary Zn supplementation enhanced lipase activity and adiponectin, which could promote triglyceride breakdown and fatty acid oxidation and lead to reduced lipid in hepatopancreas. The mRNA expressions of ob-rb, adipor, camkkβ, ampk, cd36, mcd, cpt1 involved in Zn-induced lipid catabolism were up-regulated, and expressions of srebp, acc, fas and scd1 were down-regulated. The mRNA levels of SLC39 family genes (zip3, zip9, zip11, zip14) in hepatopancreas were up-regulated with increasing dietary Zn level. The results demonstrated that dietary Zn level could significantly affect growth performance, tissue deposition of zinc, lipid metabolites and expression of genes involved in lipogenesis and lipolysis in Litopenaeus vannamei.

• Publication year

  2020

• Venue

  British Journal of Nutrition

• Publication date

  2020-05-15

• Fields of study

  Agricultural and Food Sciences, Medicine

• Identifiers
  DOI 10.1017/S0007114520001725PMID 32410717
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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