Evidence map›Paper›PMID 32537493›Full record

ArticleScience advances2020

Beneficial metabolic role of β-arrestin-1 expressed by AgRP neurons.

Sai P Pydi, Zhenzhong Cui, Zhenyan He, Luiz F Barella, Jonathan Pham, Yinghong Cui, Douglas J Oberlin, Hale Ergin Egritag, Nikhil Urs, Oksana Gavrilova and 4 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Pharmacological reviews · 2023
    Review
  4. Angiotensin ATCell reports · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Barbadin Potentiates Long-Term Effects of Lorcaserin on POMC Neurons and Weight Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Key Metabolic Functions of β-Arrestins: Studies with Novel Mouse Models.Trends in endocrinology and metabolism: TEM · 2021
    Review
  11. Review
  12. Review
  13. Review
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

14 authors at 5 institutions in 1 country.

Sai P PydiMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0001-7170-6519
Zhenzhong CuiMouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.
Zhenyan HeDivision of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Luiz F BarellaMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0003-2211-3842
Jonathan PhamMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0001-7531-4520
Yinghong CuiMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0002-9889-6655
Douglas J OberlinDiabetes, Obesity and Metabolism Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.ORCID 0000-0003-0625-5584
Hale Ergin EgritagDiabetes, Obesity and Metabolism Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
Nikhil UrsDepartment of Pharmacology and Therapeutics, University of Florida, Gainesville, FL 32610, USA.ORCID 0000-0003-1819-7836
Oksana GavrilovaMouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0002-9310-1198
Gary J SchwartzDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.ORCID 0000-0003-0446-5553
Christoph BuettnerDiabetes, Obesity and Metabolism Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
Kevin W WilliamsDivision of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.ORCID 0000-0002-8434-8658
Jürgen WessMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.ORCID 0000-0003-0818-1232
National Institute of Diabetes and Digestive and Kidney Diseases · USIcahn School of Medicine at Mount Sinai · USThe University of Texas Southwestern Medical Center · USAlbert Einstein College of Medicine · USUniversity of Florida · US

Funding

Stable Isotope and Metabolomics CoreP60DK020541 · NIDDK · YESHIVA UNIVERSITY · PI PESSIN, JEFFREY E. · 1986 to 2014
$29.8M
Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
Metabolic Studies of Mouse Models of Obesity and DiabetesZICDK070002 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GAVRILOVA, OKSANA · 2009 to 2025
$15.0M
Molecular basis of G protein-coupled receptor functionZIADK031129 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WESS, JURGEN · 2009 to 2025
$6.7M
Central Mechanisms Regulating Acute Leptin and Insulin SignalingR01DK100699 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAMS, KEVIN W · 2014 to 2018
$1.8M
Cellular and Synaptic Reorganization after Exercise TrainingR01DK119169 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAMS, KEVIN W · 2018 to 2021
$1.6M
The role of Stat3 signaling in leptin's pleitropic action.K08DK074873 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BUETTNER, CHRISTOPH · 2006 to 2009
$510k
The role of the endocannabinoid system in regulating hepatic glucose fluxesR03DK082724 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BUETTNER, CHRISTOPH · 2009 to 2010
$169k
NIDDK NIH HHS K08 DK074873NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P60 DK020541NIDDK NIH HHS R01 DK083568NIDDK NIH HHS R01 DK100699NIDDK NIH HHS R01 DK119169NIDDK NIH HHS R03 DK082724
6 · The paper itself

Abstract

β-Arrestin-1 and β-arrestin-2 have emerged as important signaling molecules that modulate glucose fluxes in several peripheral tissues. The potential roles of neuronally expressed β-arrestins in regulating glucose homeostasis remain unknown. We here report that mice lacking β-arrestin-1 (barr1) selectively in AgRP neurons displayed impaired glucose tolerance and insulin sensitivity when consuming an obesogenic diet, while mice overexpressing barr1 selectively in AgRP neurons were protected against obesity-associated metabolic impairments. Additional physiological, biochemical, and electrophysiological data indicated that the presence of barr1 is essential for insulin-mediated hyperpolarization of AgRP neurons. As a result, barr1 expressed by AgRP neurons regulates efferent neuronal pathways that suppress hepatic glucose production and promote lipolysis in adipose tissue. Mice lacking β-arrestin-2 (barr2) selectively in AgRP neurons showed no substantial metabolic phenotypes. Our data suggest that agents able to enhance the activity of barr1 in AgRP neurons may prove beneficial as antidiabetic drugs.

Identifiers

PMID32537493
PMCPMC7269658
OpenAlexW3033326837

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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.