Trk B signaling in dopamine 1 receptor neurons regulates food intake and body weight

Brittany L. Mason, Mary Kay Lobo, Luis F. Parada, Michael Lutter

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Objective Loss of BDNF-TrkB signaling results in obesity in both humans and mice; however, the neural circuit that mediates this effect is unknown. The role of TrkB signaling in dopamine-1 receptor expressing neurons in body weight regulation was tested. Methods Mice with a floxed allele of the TrkB gene were paired with mice expressing Cre-recombinase under control of the D1 promoter to conditionally knock out expression of TrkB receptors from D1-neurons. Results Deletion of TrkB receptors from D1 neurons results in obesity in chow fed mice due to increased feed efficiency. In contrast, loss of Trk B signaling in D1 neurons induced hyperphagia and hyperglycemia in mice maintained on high fat diet. Conclusions These findings indicate TrkB signaling in D1 neurons regulates body weight by distinct mechanisms for chow and high fat diet and may be important for defending the body against the development of obesity and obesity-related disorders.

Original languageEnglish (US)
Pages (from-to)2372-2376
Number of pages5
JournalObesity
Volume21
Issue number11
DOIs
StatePublished - Nov 1 2013

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

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