ArticleObesity (Silver Spring, Md.)2013
Trk B signaling in dopamine 1 receptor neurons regulates food intake and body weight.
Article in Obesity (Silver Spring, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 32 citations in OpenAlex.
- Repotrectinib: Redefining the therapeutic landscape for patients with ROS1 fusion-driven non-small cell lung cancer.Clinical and translational medicine · 2024Article
- Dysregulated Levels of Circulating Autoantibodies against Neuronal and Nervous System Autoantigens in COVID-19 Patients.Diagnostics (Basel, Switzerland) · 2023Article
- BDNF influences neural cue-reactivity to food stimuli and food craving in obesity.European archives of psychiatry and clinical neuroscience · 2021Article
- Integrated Analysis of Summary Statistics to Identify Pleiotropic Genes and Pathways for the Comorbidity of Schizophrenia and Cardiometabolic Disease.Frontiers in psychiatry · 2020Article
- Novel and ultra-rare damaging variants in neuropeptide signaling are associated with disordered eating behaviors.PloS one · 2017Article
- Ablation of TrkB expression in RGS9-2 cells leads to hyperphagic obesity.Molecular metabolism · 2013Article
- Safety of current treatment options for NTRK fusion-positive cancers.Expert opinion on drug safetyReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveLoss 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.
methodsMice 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.
resultsDeletion 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.
conclusionsThese 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.
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