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
  • Adiposity/genetics
  • Amino Acids/metabolism
  • Animals
  • Hypothalamus/metabolism
  • Insulin Resistance*/genetics
  • Male
  • Mutation
  • 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
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping