Evidence map›Paper›PMID 33631144›Full record

ArticleMetabolism: clinical and experimental2021

Global deletion of NTPDase3 protects against diet-induced obesity by increasing basal energy metabolism.

Bynvant Sandhu, Maria C Perez-Matos, Stephanie Tran, Garima Singhal, Ismail Syed, Linda Feldbrügge, Shuji Mitsuhashi, Julie Pelletier, Jinhe Huang, Yusuf Yalcin and 7 more

Open access · greenAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 21 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

17 authors at 4 institutions in 3 countries.

Bynvant SandhuDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Maria C Perez-MatosDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Stephanie TranDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Garima SinghalDivision of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Ismail SyedDivision of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Linda FeldbrüggeDepartment of Surgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Shuji MitsuhashiDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Julie PelletierCentre de recherche du CHU de Québec - Université Laval, Québec City, QC G1V 4G2, Canada.
Jinhe HuangDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Yusuf YalcinDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Eva CsizmadiaDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Shilpa Tiwari-HecklerDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Keiichi EnjyojiDivision of Hemostasis and Thrombosis, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jean SévignyCentre de recherche du CHU de Québec - Université Laval, Québec City, QC G1V 4G2, Canada; Département de microbiologie-infectiologie et d'immunologie, Faculté de Médecine, Université Laval, Québec City, QC G1V 0A6, Canada.
Eleftheria Maratos-FlierDivision of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Simon C RobsonDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; Department of Anesthesiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: srobson@bidmc.harvard.edu.
Z Gordon JiangDivision of Gastroenterology & Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: zgjiang@bidmc.harvard.edu.
Harvard University · USBeth Israel Deaconess Medical Center · USUniversité Laval · CAHumboldt-Universität zu Berlin · DE

Funding

Purinergic ThromboregulationR01HL094400 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2009 to 2010
$1.4M
Adenosine deaminase 2 regulates macrophage phenotype and liver fibrosis in nonalcoholic fatty liver diseaseK08DK115883 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JIANG, ZHENGHUI GORDON · 2018 to 2022
$839k
PGC-1α, Purines and the Postmenopausal HeartR21AG065923 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MATYAL, ROBINA, ROBSON, SIMON C. · 2021 to 2022
$481k
Directed Purinergic Signaling as Immunotherapy in LeukemiaR21CA221702 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVIGAN, DAVID E., ROBSON, SIMON C. · 2018 to 2019
$413k
CIHR PJT-156205NCI NIH HHS R21 CA221702NHLBI NIH HHS R01 HL094400NIA NIH HHS R21 AG065923NIDDK NIH HHS K08 DK115883
6 · The paper itself

Abstract

backgroundEcto-nucleoside triphosphate diphosphohydrolase 3 (NTPDase3), also known as CD39L3, is the dominant ectonucleotidase expressed by beta cells in the islet of Langerhans and on nerves. NTPDase3 catalyzes the conversion of extracellular ATP and ADP to AMP and modulates purinergic signaling. Previous studies have shown that NTPDase3 decreases insulin release from beta-cells in vitro. This study aims to determine the impact of NTPDase3 in diet-induced obesity (DIO) and metabolism in vivo.

methodsWe developed global NTPDase3 deficient (Entpd3

resultsEntpd3

conclusionsGlobal NTPDase3 deletion in mice is associated with resistance to DIO and obesity-associated glucose intolerance. This outcome is not driven by the expression of NTPDase3 in pancreatic beta-cells, but rather likely mediated through metabolic changes in adipocytes.

Indexed as

Basal MetabolismGene DeletionAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsAnimals, Genetically ModifiedBlood GlucoseDiet, High-FatDisease Models, AnimalFemaleHomeostasisInsulinInsulin-Secreting CellsMaleMiceMice, Inbred C57BLBlood GlucoseInsulinnucleoside-triphosphate diphosphohydrolase 3PyrophosphatasesAdipose tissueEctonucleotidaseInsulin resistanceNTPDase3ObesityPurinergic signaling

Identifiers

PMID33631144
PMCPMC8052311
OpenAlexW3131300091

What OpenQuestion holds

Textmetadata
LicenceTDM
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.