Lack of hypophagia in CB1 null mice is associated to decreased Hypothalamic POMC and CART

Ricardo Lage, Claudia Parisi, Patricia Seoane-Collazo, Johan Fernø, Roberta Mazza, Fátima Bosch, Luisa M. Seoane, Ruben Nogueiras, Carlos Diéguez, Carmelo Quarta, Miguel López

Research output: Contribution to journalArticleResearchpeer-review

6 Citations (Scopus)


© The Author 2015. Background: Cumulative data indicate that the endocannabinoid system plays a major role in feeding behavior and energy balance. Genetic silencing of cannabinoid receptor type 1 (CB1) reduces body weight gain, independently of food intake. Methods: In this work, we investigated whether the hypothalamic neuropeptide expression pattern supports the absence of the anorexigenic response observed under constitutive CB1 ablation, by using neuronal CB1 conditional null mice (CamK-CB1-KO) and whole body CB1 null mice (CB1-KO). Results: Our data showed that both CB1 null models display a marked decrease in proopiomelanocortin (POMC) and cocaineamphetamine-regulated transcript (CART) expression in the arcuate nucleus of the hypothalamus (ARC). Conclusions: This evidence suggests that a lack of hypophagia is associated with the suppression of ARC anorexigenic neuropeptides and that behavioral changes in food intake (or lack thereof) after constitutive CB1 ablation are likely mediated by impaired melanocortin and CART signaling in the hypothalamus.
Original languageEnglish
Pages (from-to)1-6
JournalInternational Journal of Neuropsychopharmacology
Issue number9
Publication statusPublished - 1 Jul 2015


  • CART
  • CB1
  • Food intake
  • Hypothalamus
  • POMC


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