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NPAS4 Depletion in POMC Neurons Protects From Obesity and Alters the Feeding-regulated Transcriptome in Male Mice.

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  • 1BC Children's Hospital Research Institute, Vancouver, BC,  Canada V5Z 4H4.

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Summary
This summary is machine-generated.

Neuronal PAS domain protein 4 (Npas4) normally tempers feeding responses in proopiomelanocortin (POMC) neurons. Loss of Npas4 impairs nutrient intake sensing and leads to reduced body weight during high-fat diets.

Keywords:
POMCarcuate nucleusbody weightimmediate early genesobesity

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Area of Science:

  • Neuroscience
  • Metabolism
  • Molecular Biology

Background:

  • Immediate early genes (IEGs) like Npas4 respond to stimuli.
  • Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) regulate food intake.
  • The role of Npas4 in feeding behavior and ARC function is unknown.

Purpose of the Study:

  • Investigate the role of Npas4 in POMC neurons.
  • Determine Npas4's function in regulating food intake and body weight.
  • Elucidate the molecular mechanisms by which Npas4 influences POMC neuron activity.

Main Methods:

  • Conditional knockout of Npas4 in POMC neurons of male mice.
  • High-fat diet (HFD) feeding studies.
  • Single-cell RNA sequencing (scRNA-seq) of ARC cells.
  • Cell-to-cell communication analysis.

Main Results:

  • Npas4 is induced in POMC neurons by refeeding, glucose, and HFD.
  • Npas4 knockout mice exhibit reduced body weight and food intake on HFD.
  • scRNA-seq revealed dysregulated gene expression, reduced GABA-A receptor subunits, and altered signaling inputs in knockout POMC neurons.
  • Loss of Npas4 leads to reduced inhibitory GABAergic and increased excitatory glutamatergic signaling.

Conclusions:

  • Npas4 acts to temper POMC neuron activity.
  • Npas4 is crucial for nutrient intake sensing, particularly in overnutrition states.
  • Npas4 regulates feeding behavior by modulating GABA-A receptor expression and overall transcriptional responses in POMC neurons.