Evidence map›Paper›PMID 23139353›Full record

ArticleDiabetes2013

Neuronal androgen receptor regulates insulin sensitivity via suppression of hypothalamic NF-κB-mediated PTP1B expression.

I-Chen Yu, Hung-Yun Lin, Ning-Chun Liu, Janet D Sparks, Shuyuan Yeh, Lei-Ya Fang, Lumin Chen, Chawnshang Chang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 77 citations in OpenAlex.

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  3. Sex differences in brain glucose metabolism and Alzheimer's disease risk and progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

8 authors at 2 institutions in 2 countries.

I-Chen YuGeorge Whipple Laboratory for Cancer Research, Department of Pathology, and the Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA.
Hung-Yun Lin
Ning-Chun Liu
Janet D Sparks
Shuyuan Yeh
Lei-Ya Fang
Lumin Chen
Chawnshang Chang
University of Rochester Medical Center · USChina Medical University Hospital · TW

Funding

Non-AR mediated DHT-promoted Bladder Cancer initiation and progressionR01CA155477 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2011 to 2015
$1.6M
Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155477NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Clinical investigations highlight the increased incidence of metabolic syndrome in prostate cancer (PCa) patients receiving androgen deprivation therapy (ADT). Studies using global androgen receptor (AR) knockout mice demonstrate that AR deficiency results in the development of insulin resistance in males. However, mechanisms by which AR in individual organs coordinately regulates insulin sensitivity remain unexplored. Here we tested the hypothesis that functional AR in the brain contributes to whole-body insulin sensitivity regulation and to the metabolic abnormalities developed in AR-deficient male mice. The mouse model selectively lacking AR in the central nervous system and AR-expressing GT1-7 neuronal cells were established and used to delineate molecular mechanisms in insulin signaling modulated by AR. Neuronal AR deficiency leads to reduced insulin sensitivity in middle-aged mice. Neuronal AR regulates hypothalamic insulin signaling by repressing nuclear factor-κB (NF-κB)-mediated induction of protein-tyrosine phosphatase 1B (PTP1B). Hypothalamic insulin resistance leads to hepatic insulin resistance, lipid accumulation, and visceral obesity. The functional deficiency of AR in the hypothalamus leads to male mice being more susceptible to the effects of high-fat diet consumption on PTP1B expression and NF-κB activation. These findings suggest that in men with PCa undergoing ADT, reduction of AR function in the brain may contribute to insulin resistance and visceral obesity. Pharmacotherapies targeting neuronal AR and NF-κB may be developed to combat the metabolic syndrome in men receiving ADT and in elderly men with age-associated hypogonadism.

Indexed as

AnimalsBrainCell LineDiet, High-FatGene Expression RegulationHypothalamusInsulinInsulin ResistanceLeptinLiverMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsNF-kappa BInsulinLeptinNF-kappa BProtein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, mouseReceptors, Androgen

Identifiers

PMID23139353
PMCPMC3554386
OpenAlexW2160263629

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.