PUBLICATION
Excess feeding increases adipogenesis but lowers leptin transcript abundance in zebrafish larvae
- Authors
- Thompson, W.A., Rajeswari, J.J., Holloway, A.C., Vijayan, M.M.
- ID
- ZDB-PUB-231208-10
- Date
- 2023
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 276: 109816 (Journal)
- Registered Authors
- Vijayan, Mathilakath
- Keywords
- Fat deposition, Growth, Metabolic disorder, Nile red, Obesity, Triglycerides
- MeSH Terms
-
- Adipogenesis*/genetics
- Animals
- Larva/genetics
- Leptin/genetics
- Leptin/metabolism
- Lipids
- PPAR gamma/genetics
- PPAR gamma/metabolism
- Zebrafish*/metabolism
- PubMed
- 38061616 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Citation
Thompson, W.A., Rajeswari, J.J., Holloway, A.C., Vijayan, M.M. (2023) Excess feeding increases adipogenesis but lowers leptin transcript abundance in zebrafish larvae. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 276:109816.
Abstract
Although fish exposed to municipal wastewater effluents (MWWE) show higher lipid accumulation, whether this is due to adipogenesis is unclear. The objective here was to identify molecular markers of adipogenesis in zebrafish (Danio rerio) larvae for use as high throughput screening tools for environmental contaminants, including obesogens in MWWE. Zebrafish larvae were fed a commercial diet at a maintenance level (5 % body mass) or in excess (25 or 50 % body mass) from day 6 to 30 days post-fertilization (dpf) to stimulate adipogenesis. We monitored fat accumulation and markers of lipid metabolism, including peroxisome proliferator-activated receptor γ (ppar γ), fatty acid synthase (fas), ELOVL fatty acid elongase 2 (elovl2), diacylglycerol O-acyltransferase 2 (dgat2), leptin (lepa and lepb), leptin receptor (lepr), and lipoprotein lipase (lpl). Excess feeding led to a higher growth rate, protein content and an increase in igf1 transcript abundance. Also, these larvae had higher triglyceride levels and accumulated lipids droplets in the abdominal cavity and viscera. The molecular markers of adipogenesis, including fas, elovl2, and dgat2, were upregulated, while the transcript abundance of lpl, a lipolytic gene, were transiently lower due to excess feeding. The increased adiposity seen at 30 dpf due to excess feeding coincided with a lower lep but not lepr transcript abundance in zebrafish. Our results demonstrate that excess feeding alters the developmental programming of key genes involved in lipid homeostasis, leading to excess lipid accumulation in zebrafish larvae. Overall, fas, elovl2, lpl, and dgat2, but not lep or ppar γ, have the potential as biomarkers of adipogenesis in zebrafish larvae.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping