Evidence map›Paper›PMID 34724097›Full record

ArticleCellular and molecular life sciences : CMLS2021

Role of Akt isoforms in neuronal insulin signaling and resistance.

Medha Sharma, Chinmoy Sankar Dey

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  6. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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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

2 authors at 1 institution in 1 country.

Medha SharmaKusuma School of Biological Sciences, Indian Institute of Technology-Delhi, Hauz Khas, New Delhi, 110016, India.
Chinmoy Sankar DeyKusuma School of Biological Sciences, Indian Institute of Technology-Delhi, Hauz Khas, New Delhi, 110016, India. csdey@bioschool.iitd.ac.in.ORCID http://orcid.org/0000-0003-0667-915X
Indian Institute of Technology Delhi · IN

Funding

council of scientific and industrial research, india (09/086 (1256)/2016-EMR-1)Department of Biotechnology, Government of India PR32795/MED/122/229/2019
6 · The paper itself

Abstract

The aim of the present study was to determine the role of Akt isoforms in insulin signaling and resistance in neuronal cells. By silencing Akt isoforms individually and in pairs, in Neuro-2a and HT22 cells we observed that, in insulin-sensitive condition, Akt isoforms differentially reduced activation of AS160 and glucose uptake with Akt2 playing the major role. Under insulin-resistant condition, phosphorylation of all isoforms and glucose uptake were severely affected. Over-expression of individual isoforms in insulin-sensitive and resistant cells differentially reversed AS160 phosphorylation with concomitant reversal in glucose uptake indicating a compensatory role of Akt isoforms in controlling neuronal insulin signaling. Post-insulin stimulation Akt2 translocated to the membrane the most followed by Akt3 and Akt1, decreasing glucose uptake in the similar order in insulin-sensitive cells. None of the Akt isoforms translocated in insulin-resistant cells or high-fat-diet mediated diabetic mice brain cells. Based on our data, insulin-dependent differential translocation of Akt isoforms to the plasma membrane turns out to be the key factor in determining Akt isoform specificity. Thus, isoforms play parallel with predominant role by Akt2, and compensatory yet novel role by Akt1 and Akt3 to regulate neuronal insulin signaling, glucose uptake, and insulin-resistance.

Indexed as

Insulin ResistanceAnimalsBiological TransportCell MembraneGene Expression RegulationGTPase-Activating ProteinsHippocampusHypoglycemic AgentsInsulinMiceNeuroblastomaNeuronsPhosphorylationProtein IsoformsProto-Oncogene Proteins c-aktAkt1 protein, mouseAkt2 protein, mouseAkt3 protein, mouseGTPase-Activating ProteinsHypoglycemic AgentsInsulinProtein IsoformsProto-Oncogene Proteins c-aktTbc1d4 protein, mouseAkt1Akt2Akt3AS160Neuronal insulin resistanceNeuronal insulin signaling

Identifiers

PMID34724097
PMCPMC11073101
OpenAlexW3210066609

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.