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Area of Science:

  • Genetics and Neuroscience
  • Obesity Research
  • Molecular Biology

Background:

  • Intronic polymorphisms in the FTO gene are linked to increased body weight.
  • These FTO variants may affect the expression of the nearby RPGRIP1L gene, a ciliary gene.
  • Previous research indicated that reduced RPGRIP1L in mouse Pomc neurons causes obesity via increased food intake.

Purpose of the Study:

  • To investigate the role of RPGRIP1L in Pomc neurons concerning obesity.
  • To determine the neurodevelopmental effects of RPGRIP1L deficiency in Pomc neurons.
  • To explore the impact of obesity-risk FTO alleles on RPGRIP1L expression and POMC neuron development in humans.

Main Methods:

  • Congenital and adult-onset deletion of Rpgrip1l in mouse Pomc neurons.
  • Analysis of Pomc/Npy neuronal number ratio and ARH-PVH axonal projections.
  • Assessment of cilia-positive neurons and SHH pathway responses in human iPSC-derived neurons.
  • Investigation of RPGRIP1L expression and POMC neuron numbers in human ESc-derived neurons with obesity-risk FTO alleles.

Main Results:

  • RPGRIP1L deletion in Pomc neurons led to hyperphagia and obesity, associated with reduced Pomc/Npy neuronal ratio and increased ARH-PVH projections.
  • Biallelic RPGRIP1L mutations in human neurons resulted in fewer cilia-positive neurons and diminished SHH responses.
  • Human neurons with obesity-risk FTO alleles showed decreased RPGRIP1L expression and fewer POMC neurons.
  • Overexpression of RPGRIP1L increased POMC cell number.

Conclusions:

  • Functional intronic FTO polymorphisms affect hypothalamic RPGRIP1L expression.
  • Altered RPGRIP1L expression impacts the development of POMC neurons and their projections.
  • These neurodevelopmental changes contribute to hyperphagia and increased adiposity, linking FTO variants to obesity.