PUBLICATION
Mutation of spexin2 promotes feeding, somatic growth, adiposity and insulin resistance in zebrafish
- Authors
- Zhao, T., Ye, Z., Liu, Y., Lin, H., Li, S., Zhang, Y.
- ID
- ZDB-PUB-220317-5
- Date
- 2022
- Source
- American journal of physiology. Regulatory, integrative and comparative physiology 322(5): R454-R465 (Journal)
- Registered Authors
- Keywords
- energy metabolic regulation, satiety factor, spexin2, zebrafish
- MeSH Terms
-
- Hypothalamus/metabolism
- Adiposity/genetics
- Amino Acids/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- PubMed
- 35293264 Full text @ Am. J. Physiol. Regul. Integr. Comp. Physiol.
Abstract
Spexin2 (spx2) is a newly identified gene in vertebrates, but its biological functions remain unclear. In this study, we cloned the full-length cDNA of spx2 in zebrafish. The 288 bp open reading frame encodes a protein of 95 amino acids (aa) that contains a 14 aa mature peptide. Spx2 is highly expressed in brain and testis. Its expression was significantly down-regulated in the hypothalamus after a 1 h feeding treatment and 7 days of food deprivation. Using a zebrafish spx2-/- mutant line, we observed a greater amount of food intake and changes in mRNA levels of feeding factors. We found that, SPX2 acts as a satiety factor that inhibits food intake by downregulating the expression of agouti related neuropeptide (agrp). Moreover, spx2 mutant fish exhibited a larger body size, excessive lipid accumulation, and insulin resistance. Taken together, our results revealed that SPX2 functions as a satiety factor involved in energy metabolic regulation in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping