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Atg16L1 Knockout Induces Insulin Resistance through Proteasomal IRS1 Degradation, Mediated by the Induction of ER Stress

2019· article· en· W3177128354 on OpenAlexaffabout
Scott Frendo‐Cumbo, Javier R. Jaldín‐Fincati, John H. Brumell, Amira Klip

Bibliographic record

VenueThe FASEB Journal · 2019
Typearticle
Languageen
FieldMedicine
TopicAutophagy in Disease and Therapy
Canadian institutionsHospital for Sick ChildrenUniversity of Toronto
Fundersnot available
KeywordsIRS1Insulin resistanceProtein kinase BInsulin receptorEndocrinologyInsulin receptor substrateInternal medicineInsulinAutophagyChemistryDownregulation and upregulationPhosphorylationIRS2PI3K/AKT/mTOR pathwayCell biologyBiologySignal transductionMedicineBiochemistryApoptosis

Abstract

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Insulin resistance is a defining feature of type 2 diabetes, yet our understanding of the progression and development of insulin resistance is incomplete. Recently, deficient autophagy, a bulk degradation pathway, was associated with the induction of insulin resistance, although the causative mechanism remains unknown. We sought to investigate the underlying signals responsible for how deficient autophagy induces insulin resistance. We report that knockout of an essential autophagy protein, Autophagy Related 16L1 (Atg16L1), in mouse embryonic fibroblasts (MEFs) markedly decreases insulin and insulin‐like growth factor 1 (IGF1)‐stimulated Akt recruitment to the cellular membrane and phosphorylation on S473 and T308, as well as cortical actin remodelling. Atg16L1 KO did not adversely affect insulin receptor (IR) or IGF1 receptor content, cell surface IR localization or 125 I‐insulin binding. However, Atg16L1 KO MEFs and Atg16L1 depleted HeLa cells displayed reduced protein content of Insulin Receptor Substrates (IRS1 and IRS2), pivotal proximal signals in insulin signaling known to be dysregulated in insulin resistant and diabetic states. Corroborating these findings, visceral adipose tissue of high fat‐fed mice displayed lower Atg16L1 mRNA and IRS1 protein content. Expression of IRS1myc recovered insulin‐stimulated Akt phosphorylation in KO MEFs. Treatment of KO MEFs with the proteasome inhibitor MG132restored IRS1 protein content and insulin‐stimulated Akt phosphorylation. Moreover, ER stress, which induces insulin resistance at the level of IRS1, was upregulated in Atg16L1 KO MEFs. Alleviating ER stress with the chemical chaperone phenylbutyrate increased IRS1 protein expression and insulin stimulated Akt phosphorylation similar to MG132. Together, we show that Atg16L1 KO induces insulin and IGF1 resistance through the induction of ER stress, leading to targeted proteasomal degradation of IRS1. Support or Funding Information S.F.C was supported by an NSERC Alexander Graham Bell Canada Graduate Scholarship‐Doctoral (CGS D), as well as Restracomp and a 2018 Pricewaterhouse Coopers Student Bursary from the Hospital for Sick Children. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.007

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.018
GPT teacher head0.266
Teacher spread0.248 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2019
Admission routes2
Has abstractyes

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