PUBLICATION
Glucose inhibits haemostasis and accelerates diet-induced hyperlipidaemia in zebrafish larvae
- Authors
- Morris, S., Cholan, P.M., Britton, W.J., Oehlers, S.H.
- ID
- ZDB-PUB-210926-3
- Date
- 2021
- Source
- Scientific Reports 11: 19049 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Diet*
- Egg Yolk
- Glucose/pharmacology*
- Hemostasis/drug effects*
- Hyperlipidemias/prevention & control*
- Zebrafish/growth & development*
- PubMed
- 34561530 Full text @ Sci. Rep.
Citation
Morris, S., Cholan, P.M., Britton, W.J., Oehlers, S.H. (2021) Glucose inhibits haemostasis and accelerates diet-induced hyperlipidaemia in zebrafish larvae. Scientific Reports. 11:19049.
Abstract
Hyperglycaemia damages the microvasculature in part through the reduced recruitment of immune cells and interference with platelet signalling, leading to poor wound healing and accelerated lipid deposition in mammals. We investigated the utility of zebrafish larvae to model the effect of exogenous glucose on neutrophil and macrophage recruitment to a tail wound, wound-induced haemostasis, and chicken egg yolk feed challenge-induced hyperlipidaemia by supplementing larvae with exogenous glucose by immersion or injection. Neither method of glucose supplementation affected the recruitment of neutrophils and macrophages following tail transection. Glucose injection reduced thrombocyte retention and fibrin plug formation while only thrombocyte retention was reduced by glucose immersion following tail transection. We observed accelerated lipid accumulation in glucose-injected larvae challenged with high fat chicken egg yolk feeding. Our study identifies conserved and divergent effects of high glucose on inflammation, haemostasis, and hyperlipidaemia in zebrafish larvae compared to mammals.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping