PUBLICATION
Selenium deficiency-induced high concentration of ROS restricts hypertrophic growth of skeletal muscle in juvenile zebrafish by suppressing TORC1-mediated protein synthesis
- Authors
- Wang, L., Yin, J., Liao, C., Cheng, R., Chen, F., Yu, H., Zhang, X.
- ID
- ZDB-PUB-230529-40
- Date
- 2023
- Source
- The British journal of nutrition 130(11): 1841-1851 (Journal)
- Registered Authors
- Keywords
- Selenium, protein synthesis, redox, skeletal muscle growth, zebrafish
- MeSH Terms
-
- Selenium*/deficiency
- Selenium*/pharmacology
- Zebrafish*
- Protein Biosynthesis/drug effects
- Antioxidants/pharmacology
- Signal Transduction
- Reactive Oxygen Species*/metabolism
- Animals
- Mechanistic Target of Rapamycin Complex 1*/metabolism
- Proto-Oncogene Proteins c-akt/metabolism
- Hypertrophy*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- Muscle, Skeletal*/metabolism
- PubMed
- 37246564 Full text @ Br. J. Nutr.
Citation
Wang, L., Yin, J., Liao, C., Cheng, R., Chen, F., Yu, H., Zhang, X. (2023) Selenium deficiency-induced high concentration of ROS restricts hypertrophic growth of skeletal muscle in juvenile zebrafish by suppressing TORC1-mediated protein synthesis. The British journal of nutrition. 130(11):1841-1851.
Abstract
Selenium (Se) deficiency causes impaired growth of fish skeletal muscle due to the retarded hypertrophy of muscle fibers. However, the inner mechanisms remain unclear. According to our previous researches, we infer this phenomenon is associated with Se deficiency-induced high concentration of reactive oxygen species (ROS), which could suppress the target of rapamycin complex 1 (TORC1) pathway-mediated protein synthesis by inhibiting protein kinase B (Akt), an upstream protein of TORC1. To test this hypothesis, juvenile zebrafish (45 days post fertilization) were fed a basal Se-adequate diet or a basal Se-deficient diet, or them supplemented with an antioxidant (DL-α-tocopherol acetate, designed as VE) or a TOR activator (MHY1485) for 30 days. Zebrafish fed Se-deficient diets exhibited a clear Se-deficient status in skeletal muscle, which was not influenced by dietary VE and MHY1485. Se deficiency significantly elevated ROS concentrations, inhibited Akt activity and TORC1 pathway, suppressed protein synthesis in skeletal muscle, and impaired hypertrophy of skeletal muscle fibers. However, these negative effects of Se deficiency were partly (except that on ROS concentration) alleviated by dietary MHY1485 and completely alleviated by dietary VE. These data strongly support our speculation that Se deficiency-induced high concentration of ROS exerts a clear inhibiting effect on TORC1 pathway-mediated protein synthesis by regulating Akt activity, thereby restricting the hypertrophy of skeletal muscle fibers in fish. Our findings provide a mechanistic explanation for Se deficiency-caused retardation of fish skeletal muscle growth, contributing to a better understanding of the nutritional necessity and regulatory mechanisms of Se in fish muscle physiology.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping