Evidence map›Paper›PMID 28589878›Full record

ArticleeLife2017

Distinct Akt phosphorylation states are required for insulin regulated Glut4 and Glut1-mediated glucose uptake.

Muheeb Beg, Nazish Abdullah, Fathima Shazna Thowfeik, Nasser K Altorki, Timothy E McGraw

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 162 citations in OpenAlex.

  1. Review
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  5. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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39 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Muheeb BegDepartment of Biochemistry, Weill Cornell Medicine, New York, United States.
Nazish AbdullahDepartment of Biochemistry, Weill Cornell Medicine, New York, United States.
Fathima Shazna ThowfeikDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Nasser K AltorkiDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Timothy E McGrawDepartment of Biochemistry, Weill Cornell Medicine, New York, United States.ORCID 0000-0001-9748-263X
Cornell University · US

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

Insulin, downstream of Akt activation, promotes glucose uptake into fat and muscle cells to lower postprandial blood glucose, an enforced change in cellular metabolism to maintain glucose homeostasis. This effect is mediated by the Glut4 glucose transporter. Growth factors also enhance glucose uptake to fuel an anabolic metabolism required for tissue growth and repair. This activity is predominantly mediated by the Glut1. Akt is activated by phosphorylation of its kinase and hydrophobic motif (HM) domains. We show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphorylation of the kinase domain but not mTORC2 phosphorylation of the HM domain. Nonetheless, an intact HM domain is required for Glut4-mediated glucose uptake. Whereas, Glut1-mediated glucose uptake also requires mTORC2 phosphorylation of the HM domain, demonstrating both phosphorylation-dependent and independent roles of the HM domain in regulating glucose uptake. Thus, mTORC2 links Akt to the distinct physiologic programs related to Glut4 and Glut1-mediated glucose uptake.

Indexed as

Protein Processing, Post-Translational3-Phosphoinositide-Dependent Protein KinasesGlucoseGlucose Transporter Type 1Glucose Transporter Type 4Hypoglycemic AgentsInsulinMechanistic Target of Rapamycin Complex 2PhosphorylationProto-Oncogene Proteins c-akt3-Phosphoinositide-Dependent Protein KinasesGlucoseGlucose Transporter Type 1Glucose Transporter Type 4Hypoglycemic AgentsInsulinMechanistic Target of Rapamycin Complex 2PDPK1 protein, humanProto-Oncogene Proteins c-aktSLC2A1 protein, humanSLC2A4 protein, humanAktcell biologyGlut1Glut4insulin actionmTORC2none

Identifiers

PMID28589878
PMCPMC5462539
OpenAlexW2623025796

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.