Evidence map›Paper›PMID 24327964›Full record

ArticleMolecular metabolism2013

Ablation of TrkB expression in RGS9-2 cells leads to hyperphagic obesity.

Guey-Ying Liao, Yuqing Li, Baoji Xu

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  5. Functional characterization and potential therapeutic avenues for variants in the NTRK2 gene causing developmental and epileptic encephalopathies.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2022
    Article
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  7. TrkB-expressing neurons in the dorsomedial hypothalamus are necessary and sufficient to suppress homeostatic feeding.Proceedings of the National Academy of Sciences of the United States of America · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Guey-Ying LiaoDepartment of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA ; Department of Neuroscience, The Scripps Research Institute Florida, Jupiter, FL 33458, USA.
Yuqing Li
Baoji Xu
Georgetown University Medical Center · USUniversity of Florida · US

Funding

Regulation of Energy Homeostasis by BDNFR01DK089237 · NIDDK · SCRIPPS FLORIDA · PI SIMERLY, RICHARD B, XU, BAOJI · 2011 to 2014
$2.1M
NIDDK NIH HHS R01 DK089237
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) and its cognate receptor, TrkB (tropomyosin receptor kinase B), are widely expressed in the brain where they regulate a wide variety of biological processes, including energy homeostasis. However, the specific population(s) of TrkB-expressing neurons through which BDNF governs energy homeostasis remain(s) to be determined. Using the Cre-loxP recombination system, we deleted the mouse TrkB gene in RGS9-2-expressing cells. In this mouse mutant, TrkB expression was abolished in several hypothalamic nuclei, including arcuate nucleus, dorsomedial hypothalamus, and lateral hypothalamus. TrkB expression was also abolished in a small number of cells in other brain regions, including the cerebral cortex and striatum. The mutant animals developed hyperphagic obesity with normal energy expenditure. Despite hyperglycemia under fed conditions, these animals exhibited normal fasting blood glucose levels and normal glucose tolerance. These results suggest that BDNF regulates energy homeostasis in part through TrkB-expressing neurons in the hypothalamus.

Indexed as

3V, third ventricleARC, arcuate nucleusBDNFBS, brainstemCb, cerebellumCtx, cerebral cortexDMH, dorsomedial hypothalamusHp, hippocampusHy, hypothalamusHyperphagiaHypothalamusLH, lateral hypothalamusNTS, nucleus of the solitary tractObesityPMV, ventral premammillary nucleusPVH, paraventricular hypothalamusRgs9-CreSN, substantia nigraStm, striatumTrkBTu, olfactory tubercleVMH, ventromedial hypothalamus

Identifiers

PMID24327964
PMCPMC3854990
OpenAlexW1995307068

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.