PUBLICATION
Somatostatin signalling coordinates energy metabolism allocation to reproduction in zebrafish
- Authors
- Chen, J., Zhao, W., Cao, L., Martins, R.S.T., Canário, A.V.M.
- ID
- ZDB-PUB-240730-13
- Date
- 2024
- Source
- BMC Biology 22: 163163 (Journal)
- Registered Authors
- Canário, Adelino
- Keywords
- Diabetes, Fecundity, Metabolism, Ovary, Pancreas, Trade-off, Zebrafish
- MeSH Terms
-
- Animals
- Energy Metabolism*
- Female
- Fertility
- Reproduction*/physiology
- Signal Transduction*
- Somatostatin*/genetics
- Somatostatin*/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 39075492 Full text @ BMC Biol.
Citation
Chen, J., Zhao, W., Cao, L., Martins, R.S.T., Canário, A.V.M. (2024) Somatostatin signalling coordinates energy metabolism allocation to reproduction in zebrafish. BMC Biology. 22:163163.
Abstract
Background Energy allocation between growth and reproduction determines puberty onset and fertility. In mammals, peripheral hormones such as leptin, insulin and ghrelin signal metabolic information to the higher centres controlling gonadotrophin-releasing hormone neurone activity. However, these observations could not be confirmed in lower vertebrates, suggesting that other factors may mediate the energetic trade-off between growth and reproduction. A bioinformatic and experimental study suggested co-regulation of the circadian clock, reproductive axis and growth-regulating genes in zebrafish. While loss-of-function of most of the identified co-regulated genes had no effect or only had mild effects on reproduction, no such information existed about the co-regulated somatostatin, well-known for its actions on growth and metabolism.
Results We show that somatostatin signalling is pivotal in regulating fecundity and metabolism. Knock-out of zebrafish somatostatin 1.1 (sst1.1) and somatostatin 1.2 (sst1.2) caused a 20-30% increase in embryonic primordial germ cells, and sst1.2-/- adults laid 40% more eggs than their wild-type siblings. The sst1.1-/- and sst1.2-/- mutants had divergent metabolic phenotypes: the former had 25% more pancreatic α-cells, were hyperglycaemic and glucose intolerant, and had increased adipocyte mass; the latter had 25% more pancreatic β-cells, improved glucose clearance and reduced adipocyte mass.
Conclusions We conclude that somatostatin signalling regulates energy metabolism and fecundity through anti-proliferative and modulatory actions on primordial germ cells, pancreatic insulin and glucagon cells and the hypothalamus. The ancient origin of the somatostatin system suggests it could act as a switch linking metabolism and reproduction across vertebrates. The results raise the possibility of applications in human and animal fertility.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping