Evidence map›Paper›PMID 21194385›Full record

ArticleAntioxidants & redox signaling2011

Cortical neurons develop insulin resistance and blunted Akt signaling: a potential mechanism contributing to enhanced ischemic injury in diabetes.

Bhumsoo Kim, Kelli A Sullivan, Carey Backus, Eva L Feldman

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

55 citing papers in PubMed, 91 citations in OpenAlex.

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  13. The Impact of Intermittent Hypoxia on Metabolism and Cognition.International journal of molecular sciences · 2022
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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

4 authors at 1 institution in 1 country.

Bhumsoo KimDepartment of Neurology, University of Michigan, Ann Arbor, MI 48109-2200, USA. bhumsoo@umich.edu
Kelli A Sullivan
Carey Backus
Eva L Feldman
University of Michigan–Ann Arbor · US

Funding

Lesch-Nyhan Disease: A Model for Complex Genetic, Proteomic & Metabolic PathwaysR24DK082840 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FRIEDMANN, THEODORE · 2008 to 2012
$7.3M
Mitochondrial SOD as a Target for Diabetic NeuropathyU01DK076160 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FELDMAN, EVA LUCILLE · 2006 to 2010
$1.2M
NIDDK NIH HHS R24 DK082840-01NIDDK NIH HHS U01 DK076160
6 · The paper itself

Abstract

Patients with diabetes are at higher risk of stroke and experience increased morbidity and mortality after stroke. We hypothesized that cortical neurons develop insulin resistance, which decreases neuroprotection via circulating insulin and insulin-like growth factor-I (IGF-I). Acute insulin treatment of primary embryonic cortical neurons activated insulin signaling including phosphorylation of the insulin receptor, extracellular signal-regulated kinase (ERK), Akt, p70S6K, and glycogen synthase kinase-3β (GSK-3β). To mimic insulin resistance, cortical neurons were chronically treated with 25 mM glucose, 0.2 mM palmitic acid (PA), or 20 nM insulin before acute exposure to 20 nM insulin. Cortical neurons pretreated with insulin, but not glucose or PA, exhibited blunted phosphorylation of Akt, p70S6K, and GSK-3β with no change detected in ERK. Inhibition of the phosphatidylinositol 3-kinase (PI3-K) pathway during insulin pretreatment restored acute insulin-mediated Akt phosphorylation. Cortical neurons in adult BKS-db/db mice exhibited higher basal Akt phosphorylation than BKS-db(+) mice and did not respond to insulin. Our results indicate that prolonged hyperinsulinemia leads to insulin resistance in cortical neurons. Decreased sensitivity to neuroprotective ligands may explain the increased neuronal damage reported in both experimental models of diabetes and diabetic patients after ischemia-reperfusion injury.

Indexed as

AnimalsBlotting, WesternButadienesCells, CulturedCerebral CortexChromonesEnzyme InhibitorsFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaImmunohistochemistryInsulinInsulin-Like Growth Factor IInsulin ResistanceMorpholinesNeurons2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneButadienesChromonesEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseGsk3b protein, ratInsulinInsulin-Like Growth Factor IMorpholinesNitrilesProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaU 0126

Identifiers

PMID21194385
PMCPMC3078499
OpenAlexW2055476783

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.