Dietary chromium modulates glucose homeostasis and induces oxidative stress in Pacific white shrimp (Litopenaeus vannamei)
Creators
- 1. Laboratory of Fish and Shellfish Nutrition, School of Marine Sciences, Ningbo University, Ningbo, 315211 (China)
- 2. Institute of Aquaculture, Faculty of Natural Sciences, University of Stirling, Stirling FK9 4LA, Scotland (United Kingdom)
- 3. Guangdong Provincial Key Laboratory of Marine Biotechnology, Institute of Marine Sciences, Shantou University, Shantou 515063 (China)
- 4. Zinpro Corporation, Eden Prairie, Minnesota (United States)
Description
Highlights: • Optimal dietary chromium (1.22 mg/kg) improved growth of L. vannamei. • Chromium trigger glycolysis and glycogenesis and suppress gluconeogenesis to maintain glucose homeostasis. • Excess chromium (1.63 mg/kg) caused oxidative damage and apoptosis in L. vannamei. While chromium (Cr) has been recognized as an essential nutrient for all animals, and dietary supplementation can be beneficial, it can also be toxic. The present study aimed to investigate the contrasting effects of dietary chromium in Pacific white shrimp Litopenaeus vannamei. Five experimental diets were formulated to contain Cr at levels of 0.82 (Cr0.82, unsupplemented diet), 1.01 (Cr1.01), 1.22 (Cu1.22), 1.43 (Cr1.43) and 1.63 (Cr1.63) mg/kg and were fed to shrimp for 8 weeks. Highest weight gain was recorded in shrimp fed the diet containing 1.22 mg/kg Cr. Shrimp fed the diet containing the highest level of Cr (1.63 mg/kg) showed the lowest weight gain and clear signs of oxidative stress and apoptosis as evidenced by higher levels of H2O2, malondialdehyde and 8-hydroxydeoxyguanosine, and expression of caspase 2, 3, 5, and lower contents of total and oxidized glutathione, and expression of Cu/Zn sod, cat, gpx, mt, bcl2. Chromium supplementation promoted glycolysis and inhibited gluconeogenesis as shown by increased activities of hexokinase, phosphofructokinase and pyruvate kinase, and reduced activity of phosphoenolpyruvate carboxykinase in shrimp fed the diet containing 1.43 mg/kg Cr. Shrimp fed the diet with 1.63 mg/kg Cr had lowest contents of crustacean hyperglycemic hormone and insulin like peptide in hemolymph. Expression of genes involved in insulin signaling pathway and glycose metabolism including insr, irs1, pik3ca, pdpk1, akt, acc1, gys, glut1, pk, hk were up-regulated, and foxO1, gsk-3β, g6pc, pepck were down-regulated in shrimp fed the diets supplemented with Cr. This study demonstrated that optimum dietary supplementation of Cr had beneficial effects on glucose homeostasis and growth, whereas excess caused oxidative damage and impaired growth. The results contribute to our understanding of the biological functions of chromium in shrimp.
Availability note (English)
Available from http://dx.doi.org/10.1016/j.aquatox.2021.105967Additional details
Identifiers
- DOI
- 10.1016/j.aquatox.2021.105967;
- PII
- S0166445X21002265;
Publishing Information
- Journal Title
- Aquatic Toxicology
- Journal Volume
- 240
- Journal Page Range
- vp.
- ISSN
- 0166-445X
- CODEN
- AQTODG
INIS
- Country of Publication
- Netherlands
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 53108985
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- APOPTOSIS; BIOLOGICAL FUNCTIONS; CHROMIUM; GLUCOSE; GLUTATHIONE; GLYCOLYSIS; HEXOKINASE; HOMEOSTASIS; HYDROGEN PEROXIDE; INSULIN; NUTRIENTS; OXIDATION; PHOSPHOENOLPYRUVATE; SHRIMP; SUPEROXIDE DISMUTASE; TOXICITY
- Descriptors DEC
- ALDEHYDES; ANIMALS; AQUATIC ORGANISMS; ARTHROPODS; CARBOHYDRATES; CHEMICAL REACTIONS; CRUSTACEANS; DECAPODS; DECOMPOSITION; DRUGS; ELEMENTS; ENZYMES; HEXOSES; HORMONES; HYDROGEN COMPOUNDS; INVERTEBRATES; METABOLISM; METALS; MONOSACCHARIDES; ORGANIC COMPOUNDS; OXIDOREDUCTASES; OXYGEN COMPOUNDS; PEPTIDE HORMONES; PEPTIDES; PEROXIDES; PHOSPHORUS-GROUP TRANSFERASES; PHOSPHOTRANSFERASES; POLYPEPTIDES; PROTEINS; RADIOPROTECTIVE SUBSTANCES; RESPONSE MODIFYING FACTORS; SACCHARIDES; TRANSFERASES; TRANSITION ELEMENTS
Optional Information
- Copyright
- Copyright (c) 2021 Elsevier B.V. All rights reserved.