PUBLICATION
CRISPR/Cas9-induced LEAP2 and GHSR1a knockout mutant zebrafish displayed abnormal growth and impaired lipid metabolism
- Authors
- Fei, Y., Bao, Z., Wang, Q., Zhu, Y., Lu, J., Ouyang, L., Hu, Q., Zhou, Y., Chen, L.
- ID
- ZDB-PUB-240604-6
- Date
- 2024
- Source
- General and comparative endocrinology 355: 114563 (Journal)
- Registered Authors
- Chen, Liangbiao
- Keywords
- Blood glucose, Fat, GHSR1a, LEAP2, Zebrafish
- MeSH Terms
-
- Animals
- CRISPR-Cas Systems*/genetics
- Female
- Lipid Metabolism*/genetics
- Male
- Mutation
- Receptors, Ghrelin*/genetics
- Receptors, Ghrelin*/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 38830459 Full text @ Gen. Comp. Endocrinol.
Citation
Fei, Y., Bao, Z., Wang, Q., Zhu, Y., Lu, J., Ouyang, L., Hu, Q., Zhou, Y., Chen, L. (2024) CRISPR/Cas9-induced LEAP2 and GHSR1a knockout mutant zebrafish displayed abnormal growth and impaired lipid metabolism. General and comparative endocrinology. 355:114563.
Abstract
Investigating the principles of fish fat deposition and conducting related research are current focal points in fish nutrition. This study explores the endocrine regulation of LEAP2 and GHSR1a in zebrafish by constructing mutant models and examining the effects of the endocrine factors LEAP2 and its receptor GHSR1a on zebrafish growth, feeding, and liver fat deposition. Compared to the wild type (WT), the mutation of LEAP2 results in increased feeding and decreased swimming in zebrafish. The impact is more pronounced in adult female zebrafish, characterized by increased weight, length, width, and accumulation of lipid droplets in the liver.Incontrast, deficiency in GHSR1a significantly reduces the growth of male zebrafish and markedly decreases liver fat deposition.These research findings indicate the crucial roles of LEAP2 and GHSR1a in zebrafish feeding, growth, and intracellular fat metabolism. This study, for the first time, investigated the endocrine metabolic regulation functions of LEAP2 and GHSR1a in the model organism zebrafish, providing initial insights into their effects and potential mechanisms on zebrafish fat metabolism.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping