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Hypothalamic CREB Regulates the Expression of Pomc-Processing Enzyme Pcsk2.

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Dietary fats impact hypothalamic CREB, a key regulator of energy balance. Inhibiting CREB in obesity increases body mass and reduces energy expenditure by altering proopiomelanocortin neuron function.

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Area of Science:

  • Neuroscience
  • Metabolism
  • Molecular Biology

Background:

  • Hypothalamic proopiomelanocortin (Pomc) neurons regulate energy homeostasis.
  • Dietary fats disrupt Pomc endopeptidase activity, affecting neurotransmitter production and energy balance in obesity.
  • The role of cAMP response element-binding protein (CREB) in mediating these dietary fat effects on Pomc endopeptidases was previously unknown.

Purpose of the Study:

  • To investigate the impact of a high-fat diet (HFD) on hypothalamic CREB expression and function.
  • To determine CREB's role in regulating the melanocortinergic system under HFD conditions.
  • To elucidate the molecular mechanisms linking dietary fats, CREB, and energy balance.

Main Methods:

  • Single-cell RNA sequencing analysis.
  • Quantitative PCR, immunoblotting, ELISA, and immunofluorescence assays.
  • Inhibition of hypothalamic CREB using short-hairpin RNA lentiviral vectors.

Main Results:

  • CREB is expressed and activated in arcuate nucleus Pomc neurons within nine hours of HFD introduction.
  • CREB inhibition led to increased diet-induced body mass gain and reduced energy expenditure.
  • CREB inhibition decreased the expression of Pomc endopeptidase (Pcsk2) and abolished the HFD-induced suppression of α-MSH production.

Conclusions:

  • This study provides the first evidence that CREB is involved in the dysregulation of the hypothalamic Pomc endopeptidase system during experimental obesity.
  • CREB acts as a crucial mediator linking dietary fat intake to altered energy balance through the melanocortinergic system.
  • Targeting CREB may offer a therapeutic strategy for managing obesity and metabolic dysfunction.