A novel form of ciliopathy underlies hyperphagia and obesity in Ankrd26 knockout mice

Peter Acs, Peter O. Bauer, Balazs Mayer, Tapan Bera, Rhonda Macallister, Eva Mezey, Ira Pastan

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Human ciliopathies are genetic disorders caused by mutations in genes responsible for the formation and function of primary cilia. Some are associated with hyperphagia and obesity (e.g., Bardet–Biedl Syndrome, Alström Syndrome), but the mechanisms underlying these problems are not fully understood. The human gene ANKRD26 is located on 10p12, a locus that is associated with some forms of hereditary obesity. Previously, we reported that disruption of this gene causes hyperphagia, obesity and gigantism in mice. In the present study, we looked for the mechanisms that induce hyperphagia in the Ankrd26−/− mice and found defects in primary cilia in regions of the central nervous system that control appetite and energy homeostasis.

Original languageEnglish (US)
Pages (from-to)1511-1528
Number of pages18
JournalBrain Structure and Function
Volume220
Issue number3
DOIs
StatePublished - May 1 2015
Externally publishedYes

Keywords

  • ANKRD26
  • Arcuate nucleus
  • CRH
  • Ciliary body proteins
  • Feeding behavior
  • Leptin receptor
  • Melanocortin receptor
  • Neuronal cilia
  • Obesity
  • Paraventricular nucleus

ASJC Scopus subject areas

  • Anatomy
  • Neuroscience(all)
  • Histology

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