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Unveiling the transcriptome alteration of POMC neuron in diet-induced obesity

Peng Lyu1, Zhishun Huang1, Qingjun Feng1

  • 1College of Biological Science and Engineering, Fuzhou University, Fuzhou, 350108, China.

Experimental Cell Research
|January 20, 2020
PubMed

Insights

Diet-induced obesity involves arcuate nucleus neuron imbalance. Targeting pRb phosphorylation in POMC neurons offers a potential therapeutic strategy for obesity.

Area of Science:

  • Neuroscience
  • Metabolic disease research
  • Molecular biology

Background:

  • Loss of neuron homeostasis in the arcuate nucleus (ARC) contributes to diet-induced obesity (DIO).
  • Previous work indicated Rb1 gene loss disrupts anorexigenic POMC neuron homeostasis and causes obesity in mice.

Purpose of the Study:

  • To investigate transcriptomic alterations in POMC neurons during DIO development.
  • To identify molecular pathways involved in DIO pathogenesis.
  • To explore pRb phosphorylation as a potential therapeutic target for DIO.

Main Methods:

  • Transcriptomic profiling (RNA-seq) of POMC neurons from DIO mice fed a high-fat diet (HFD).
  • Pathway enrichment analysis of differentially expressed genes (DEGs).
  • Validation of pRb protein phosphorylation and intervention via stereotaxic delivery of unphosphorylated pRbΔP.

Main Results:

  • 1066 differentially expressed genes (DEGs) were identified in POMC neurons.
  • Key pathways implicated in DIO include cell cycle, apoptosis, chemokine signaling, and sphingolipid metabolism.
  • HFD feeding inactivated pRb via phosphorylation in POMC neurons; intervention reversed DIO.

Conclusions:

  • Dysregulation of cell cycle and other pathways in POMC neurons contributes to DIO.
  • pRb phosphorylation is a critical event in DIO development.
  • Targeting pRb phosphorylation presents a promising therapeutic avenue for treating obesity.
Keywords:
Diet-induced obesity (DIO)High-fat-diet (HFD)Neuron homeostasisPOMC neuronpRb phosphorylation

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