Evidence map›Paper›PMID 33239450›Full record

ArticleDiabetes2021

Glucagon Resistance and Decreased Susceptibility to Diabetes in a Model of Chronic Hyperglucagonemia.

Nadejda Bozadjieva Kramer, Camila Lubaczeuski, Manuel Blandino-Rosano, Grant Barker, George K Gittes, Alejandro Caicedo, Ernesto Bernal-Mizrachi

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 30 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

7 authors at 3 institutions in 1 country.

Nadejda Bozadjieva KramerDepartment of Medicine, University of Michigan Medical Center, Ann Arbor, MI.
Camila LubaczeuskiDivision of Endocrinology, Metabolism and Diabetes, Department of Internal Medicine, Miller School of Medicine, University of Miami, Miami, FL.
Manuel Blandino-RosanoDepartment of Medicine, University of Michigan Medical Center, Ann Arbor, MI.
Grant BarkerDivision of Endocrinology, Metabolism and Diabetes, Department of Internal Medicine, Miller School of Medicine, University of Miami, Miami, FL.
George K GittesUPMC Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburg, PA.
Alejandro CaicedoDivision of Endocrinology, Metabolism and Diabetes, Department of Internal Medicine, Miller School of Medicine, University of Miami, Miami, FL.ORCID 0000-0002-3765-3529
Ernesto Bernal-MizrachiDivision of Endocrinology, Metabolism and Diabetes, Department of Internal Medicine, Miller School of Medicine, University of Miami, Miami, FL ebernalm@med.miami.edu.ORCID 0000-0001-9997-3301
University of Miami · USUniversity of Michigan · USUniversity of Pittsburgh · US

Funding

Michigan Institute for Clinical and Health Research (MICHR)UL1TR002240 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, JULIE C, MASHOUR, GEORGE ALEXANDER · 2017 to 2022
$54.9M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WILLIAM H HERMAN · 2013 to 2026
$24.3M
CELLULAR AND MOLECULAR BIOLOGY AT MICHIGANT32GM007315 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTHENVEEDU, MANOJKUMAR A · 1985 to 2021
$12.8M
AKT/mTOR Signaling and Regulation of Cell Cycle in beta CellsR01DK073716 · NIDDK · WASHINGTON UNIVERSITY · PI BERNAL-MIZRACHI, ERNESTO · 2006 to 2022
$4.6M
Nutrient Signals and Programming of Pancreas DevelopmentR01DK084236 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERNAL-MIZRACHI, ERNESTO · 2010 to 2018
$2.9M
Obesity Surgery Scientist Training ProgramT32DK108740 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Justin Brigham Dimick, RANDY J SEELEY · 2016 to 2026
$2.2M
mTOR signaling and regulation of alpha-cell mass and functionI01BX002728 · VA · MIAMI VA HEALTH CARE SYSTEM · PI BERNAL-MIZRACHI, ERNESTO · 2016 to 2025
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BLRD VA I01 BX002728NCATS NIH HHS UL1 TR002240NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK073716NIDDK NIH HHS R01 DK084236NIDDK NIH HHS T32 DK108740NIGMS NIH HHS T32 GM007315
6 · The paper itself

Abstract

Elevation of glucagon levels and increase in α-cell mass are associated with states of hyperglycemia in diabetes. Our previous studies have highlighted the role of nutrient signaling via mTOR complex 1 (mTORC1) regulation that controls glucagon secretion and α-cell mass. In the current studies we investigated the effects of activation of nutrient signaling by conditional deletion of the mTORC1 inhibitor, TSC2, in α-cells (αTSC2

Indexed as

AnimalsBlood GlucoseBody WeightDisease Models, AnimalDisease SusceptibilityEatingGlucagonGlucagon-Like Peptide 1Glucagon-Secreting CellsGlucose IntoleranceInsulinInsulin SecretionMechanistic Target of Rapamycin Complex 1MiceReceptors, GlucagonSignal TransductionBlood GlucoseGlucagonGlucagon-Like Peptide 1InsulinMechanistic Target of Rapamycin Complex 1Receptors, GlucagonTsc2 protein, mouseTuberous Sclerosis Complex 2 Protein

Identifiers

PMID33239450
PMCPMC7881862
OpenAlexW3034529715

What OpenQuestion 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 OpenQuestion graph.