Conditional deletion of neurogenin-3 using Nkx2.1iCre results in a mouse model for the central control of feeding, activity and obesity - Archive ouverte HAL Access content directly
Journal Articles Disease Models & Mechanisms Year : 2013

Conditional deletion of neurogenin-3 using Nkx2.1iCre results in a mouse model for the central control of feeding, activity and obesity

Neal Anthwal
  • Function : Author
Michelle Pelling
  • Function : Author
Suzanne Claxton
  • Function : Author
Georg Mellitzer
  • Function : Author
Caitlin Collin
  • Function : Author
Nicoletta Kessaris
  • Function : Author
William D Richardson
  • Function : Author
Siew-Lan Ang
  • Function : Author
  • PersonId : 1231790

Abstract

Summary The ventral hypothalamus acts to integrate visceral and systemic information to control energy balance. The basic helix-loop-helix transcription factor neurogenin-3 (Ngn3) is required for pancreatic β-cell development and has been implicated in neuronal development in the hypothalamus. Here, we demonstrate that early embryonic hypothalamic inactivation of Ngn3 (also known as Neurog3)in mice results in rapid post-weaning obesity that is associated with hyperphagia and reduced energy expenditure. This obesity is caused by loss of expression of Pomc in Pomc- and Cart-expressing (Pomc/Cart) neurons in the arcuate nucleus, indicating an incomplete specification of anorexigenic first order neurons. Furthermore, following the onset of obesity, both the arcuate and ventromedial hypothalamic nuclei become insensitive to peripheral leptin treatment. This conditional mouse mutant therefore represents a novel model system for obesity that is associated with hyperphagia and underactivity, and sheds new light upon the roles of Ngn3 in the specification of hypothalamic neurons controlling energy balance.
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hal-04006946 , version 1 (27-02-2023)

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Neal Anthwal, Michelle Pelling, Suzanne Claxton, Georg Mellitzer, Caitlin Collin, et al.. Conditional deletion of neurogenin-3 using Nkx2.1iCre results in a mouse model for the central control of feeding, activity and obesity. Disease Models & Mechanisms, 2013, ⟨10.1242/dmm.011916⟩. ⟨hal-04006946⟩
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