Evidence map›Paper›PMID 34644106›Full record

ArticleScience advances2021

GLUT4-overexpressing engineered muscle constructs as a therapeutic platform to normalize glycemia in diabetic mice.

Margarita Beckerman, Chava Harel, Inbal Michael, Amira Klip, Philip J Bilan, Emily J Gallagher, Derek LeRoith, Eli C Lewis, Eddy Karnieli, Shulamit Levenberg

Abstract read
In one paragraph

Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

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  13. Biophysics reviews · 2022
    Review
  14. 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

10 authors.

Margarita BeckermanFaculty of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0003-3318-3985
Chava HarelRina and Avner Schneur Center of Diabetes Research, Technion-Israel Institute of Technology, Haifa, Israel.
Inbal MichaelFaculty of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.
Amira KlipProgram in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.ORCID 0000-0001-7906-0302
Philip J BilanProgram in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.ORCID 0000-0002-4171-9316
Emily J GallagherDivision of Endocrinology, Diabetes and Bone Diseases, Samuel Bronfman Department of Medicine, Ichan School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0002-7920-8474
Derek LeRoithDivision of Endocrinology, Diabetes and Bone Diseases, Samuel Bronfman Department of Medicine, Ichan School of Medicine at Mount Sinai, New York, NY 10029, USA.
Eli C LewisDepartment of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Eddy KarnieliRina and Avner Schneur Center of Diabetes Research, Technion-Israel Institute of Technology, Haifa, Israel.
Shulamit LevenbergFaculty of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0001-5471-7339

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
Mechanisms for the pro-metastatic effects of hyperinsulinemia on breast cancerR01CA128799 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEROITH, DEREK · 2008 to 2018
$3.7M
Cholesterol promotes breast cancer progression: establishing the mechanismsK08CA190770 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GALLAGHER, EMILY JANE · 2014 to 2018
$843k
NCI NIH HHS K08 CA190770NCI NIH HHS R01 CA128799NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P60 DK020541
6 · The paper itself

Abstract

Skeletal muscle insulin resistance is a main defect in type 2 diabetes (T2D), which is associated with impaired function and content of glucose transporter type 4 (GLUT4). GLUT4 overexpression in skeletal muscle tissue can improve glucose homeostasis. Therefore, we created an engineered muscle construct (EMC) composed of GLUT4-overexpressing (OEG4) cells. The ability of the engineered implants to reduce fasting glucose levels was tested in diet-induced obesity mice. Decrease and stabilization of basal glucose levels were apparent up to 4 months after implantation. Analysis of the retrieved constructs showed elevated expression of myokines and proteins related to metabolic processes. In addition, we validated the efficiency of OEG4-EMCs in insulin-resistant mice. Following high glucose load administration, mice showed improved glucose tolerance. Our data indicate that OEG4-EMC implant is an efficient mode for restoring insulin sensitivity and improving glucose homeostasis in diabetic mice. Such procedure is a potential innovative modality for T2D therapy.

Identifiers

PMID34644106
PMCPMC8514095

What OpenQuestion holds

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Registered trials

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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.