Evidence map›Paper›PMID 25830096›Full record

ArticleMolecular metabolism2015

Angiotensin type 1a receptors in the forebrain subfornical organ facilitate leptin-induced weight loss through brown adipose tissue thermogenesis.

Colin N Young, Donald A Morgan, Scott D Butler, Kamal Rahmouni, Susan B Gurley, Thomas M Coffman, Allyn L Mark, Robin L Davisson

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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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 3 institutions in 1 country.

Colin N YoungBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Donald A MorganDepartment of Pharmacology, University of Iowa, Iowa City, IA, 52242, USA.
Scott D ButlerBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Kamal RahmouniDepartment of Pharmacology, University of Iowa, Iowa City, IA, 52242, USA.
Susan B GurleyDivision of Nephrology, Department of Medicine, Duke University, Durham, NC 27710, USA.
Thomas M CoffmanDivision of Nephrology, Department of Medicine, Duke University, Durham, NC 27710, USA.
Allyn L MarkDepartment of Internal Medicine, University of Iowa, Iowa City, IA, 52242, USA ; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, NY, 10065, USA.
Robin L DavissonBiomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA ; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, NY, 10065, USA.
Cornell University · USDuke University · USUniversity of Iowa · US

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI GROBE, JUSTIN L · 2007 to 2022
$30.2M
TARGETED ABLATION OF BRAIN ANGIOTENSINGERGIC SYSTEMSR01HL063887 · NHLBI · UNIVERSITY OF IOWA · PI DAVISSON, ROBIN L · 2000 to 2014
$4.4M
Role of Central Neural NFkB and ER Stress in Obesity-induced HypertensionR00HL116776 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI YOUNG, COLIN NEAL · 2015 to 2017
$747k
Role of Central Neural NFkB and ER Stress in Obesity-induced HypertensionK99HL116776 · NHLBI · CORNELL UNIVERSITY · PI YOUNG, COLIN NEAL · 2013 to 2014
$174k
NHLBI NIH HHS K99 HL116776NHLBI NIH HHS P01 HL084207NHLBI NIH HHS R00 HL116776NHLBI NIH HHS R01 HL063887
6 · The paper itself

Abstract

objectiveElevations in brain angiotensin-II cause increased energy expenditure and a lean phenotype. Interestingly, the metabolic effects of increased brain angiotensin-II mimic the actions of leptin, suggesting an interaction between the two systems. Here we demonstrate that angiotensin-type 1a receptors (AT1aR) in the subfornical organ (SFO), a forebrain structure emerging as an integrative metabolic center, play a key role in the body weight-reducing effects of leptin via brown adipose tissue (BAT) thermogenesis.

methodsCre/LoxP technology coupled with targeted viral delivery to the SFO in a mouse line bearing a conditional allele of the Agtr1a gene was utilized to determine the interaction between leptin and SFO AT1aR in metabolic regulation.

resultsSelective deletion of AT1aR in the SFO attenuated leptin-induced weight loss independent of changes in food intake or locomotor activity. This was associated with diminished leptin-induced increases in core body temperature, blunted upregulation of BAT thermogenic markers, and abolishment of leptin-mediated sympathetic activation to BAT.

conclusionsThese data identify a novel interaction between angiotensin-II and leptin in the control of BAT thermogenesis and body weight, and highlight a previously unrecognized role for the forebrain SFO in metabolic regulation.

Indexed as

Ang-II, angiotensin-IIAngiotensinAT1aR, angiotensin type 1a receptorBAT, brown adipose tissueBrainBrown adipose tissueCNS, central nervous systemLepRb, leptin receptorLeptinMetabolic regulationOVLT, organum vasculosum lamina terminalisRAS, renin-angiotensin systemSFO, subfornical organSNA, sympathetic nerve activitySympathetic nervous system

Identifiers

PMID25830096
PMCPMC4354922
OpenAlexW2128137478

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.