PUBLICATION

Cannabinoid receptor signaling regulates liver development and metabolism

Authors
Liu, L.Y., Alexa, K., Cortes, M., Schatzman-Bone, S., Kim, A.J., Mukhopadhyay, B., Cinar, R., Kunos, G., North, T.E., Goessling, W.
ID
ZDB-PUB-160218-3
Date
2016
Source
Development (Cambridge, England)   143: 609-22 (Journal)
Registered Authors
Goessling, Wolfram, North, Trista, Schatzman-Bone, Steph
Keywords
Cannabinoid receptor, Liver development, Methionine, Mouse, Zebrafish
MeSH Terms
  • Animals
  • Cannabinoids/metabolism
  • Cell Count
  • Cell Proliferation/drug effects
  • Cysteine/pharmacology
  • Hepatocytes/cytology
  • Hepatocytes/drug effects
  • Hepatocytes/metabolism
  • Liver/drug effects
  • Liver/embryology*
  • Liver/metabolism*
  • Metabolomics
  • Methionine/metabolism
  • Mutation/genetics
  • Organ Size/drug effects
  • Receptor, Cannabinoid, CB1/metabolism*
  • Receptor, Cannabinoid, CB2/metabolism*
  • Signal Transduction*/drug effects
  • Stem Cells/cytology
  • Stem Cells/drug effects
  • Stem Cells/metabolism
  • Zebrafish/embryology*
  • Zebrafish/metabolism*
  • Zebrafish Proteins/metabolism*
PubMed
26884397 Full text @ Development
CTD
26884397
Abstract
Endocannabinoid (EC) signaling mediates psychotropic effects and regulates appetite. By contrast, potential roles in organ development and embryonic energy consumption remain unknown. Here, we demonstrate that genetic or chemical inhibition of cannabinoid receptor (Cnr) activity disrupts liver development and metabolic function in zebrafish (Danio rerio), impacting hepatic differentiation, but not endodermal specification: loss of cannabinoid receptor 1 (cnr1) and cnr2 activity leads to smaller livers with fewer hepatocytes, reduced liver-specific gene expression and proliferation. Functional assays reveal abnormal biliary anatomy and lipid handling. Adult cnr2 mutants are susceptible to hepatic steatosis. Metabolomic analysis reveals reduced methionine content in Cnr mutants. Methionine supplementation rescues developmental and metabolic defects in Cnr mutant livers, suggesting a causal relationship between EC signaling, methionine deficiency and impaired liver development. The effect of Cnr on methionine metabolism is regulated by sterol regulatory element-binding transcription factors (Srebfs), as their overexpression rescues Cnr mutant liver phenotypes in a methionine-dependent manner. Our work describes a novel developmental role for EC signaling, whereby Cnr-mediated regulation of Srebfs and methionine metabolism impacts liver development and function.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Mapping