Evidence map›Paper›PMID 32228320›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2020

The neuronal (pro)renin receptor and astrocyte inflammation in the central regulation of blood pressure and blood glucose in mice fed a high-fat diet.

Caleb J Worker, Wencheng Li, Cheng-Yuan Feng, Lucas A C Souza, Ariana Julia B Gayban, Silvana G Cooper, Sanzida Afrin, Samantha Romanick, Bradley S Ferguson, Yumei Feng Earley

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-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

20 citing papers in PubMed, 28 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

10 authors at 3 institutions in 1 country.

Caleb J WorkerDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.
Wencheng LiDepartment of Pathology, Wake Forest University, Winston-Salem, North Carolina.
Cheng-Yuan FengDepartment of Neurology, Loma Linda University, Loma Linda, California.
Lucas A C SouzaDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.
Ariana Julia B GaybanDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.
Silvana G CooperDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.
Sanzida AfrinDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.
Samantha RomanickCenter for Molecular and Cellular Signal Transduction in the Cardiovascular System, University of Nevada, Reno, Nevada.
Bradley S FergusonCenter for Molecular and Cellular Signal Transduction in the Cardiovascular System, University of Nevada, Reno, Nevada.
Yumei Feng EarleyDepartment of Pharmacology and Physiology and Cell Biology, University of Nevada, Reno, School of Medicine, Reno, Nevada.ORCID 0000-0002-4138-0105
University of Nevada, Reno · USLoma Linda University · USWake Forest University · US

Funding

Transgenic Animal Genotyping and Phenotyping CoreP20GM130459 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Nathan Grainger · 2019 to 2026
$20.3M
Mouse Metabolic Phenotyping Center (MMPC) at UC DavisU2CDK092993 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LLOYD, KC KENT · 2016 to 2021
$5.9M
TRP Channel-Dependent Regulation of Arterial Tone (Renewal)R01HL091905 · NHLBI · UNIVERSITY OF NEVADA RENO · PI EARLEY, SCOTT · 2009 to 2020
$5.1M
The Neural Mechanisms of HypertensionR01HL122770 · NHLBI · UNIVERSITY OF ROCHESTER · PI FENG EARLEY, YUMEI · 2015 to 2023
$4.2M
American Heart Association-American Stroke Association 17IRG33370128NHLBI NIH HHS R01 HL091905NHLBI NIH HHS R01 HL122770NIDDK NIH HHS U2C DK092993NIGMS NIH HHS P20 GM130459
6 · The paper itself

Abstract

We report here that the neuronal (pro)renin receptor (PRR), a key component of the brain renin-angiotensin system (RAS), plays a critical role in the central regulation of high-fat-diet (HFD)-induced metabolic pathophysiology. The neuronal PRR is known to mediate formation of the majority of angiotensin (ANG) II, a key bioactive peptide of the RAS, in the central nervous system and to regulate blood pressure and cardiovascular function. However, little is known about neuronal PRR function in overnutrition-related metabolic physiology. Here, we show that PRR deletion in neurons reduces blood pressure, neurogenic pressor activity, and fasting blood glucose and improves glucose tolerance without affecting food intake or body weight following a 16-wk HFD. Mechanistically, we found that a HFD increases levels of the PRR ligand (pro)renin in the circulation and hypothalamus and of ANG II in the hypothalamus, indicating activation of the brain RAS. Importantly, PRR deletion in neurons reduced astrogliosis and activation of the astrocytic NF-κB p65 (RelA) in the arcuate nucleus and the ventromedial nucleus of the hypothalamus. Collectively, our findings indicate that the neuronal PRR plays essential roles in overnutrition-related metabolic pathophysiology.

Indexed as

AnimalsAstrocytesBlood GlucoseBlood PressureBody WeightDiet, High-FatEatingHypothalamusInflammationMiceMice, KnockoutNeuronsProrenin ReceptorReceptors, Cell SurfaceReninBlood GlucoseProrenin ReceptorReceptors, Cell SurfaceReninastrocyte inflammationdiet-induced diabetesneural mechanism(pro)renin receptorrenin-angiotensin system

Identifiers

PMID32228320
PMCPMC7272727
OpenAlexW3013295991

What Socratic 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 Socratic graph.