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Autophagy‐Related Protein 16L1 (Atg16L1) Depletion Induces Insulin Resistance Through Decreased IRS Expression

2018· article· en· W3176530220 on OpenAlexaff
Scott Frendo‐Cumbo, Javier R. Jaldín‐Fincati, John H. Brumell, Amira Klip

Bibliographic record

VenueThe FASEB Journal · 2018
Typearticle
Languageen
FieldMedicine
TopicAutophagy in Disease and Therapy
Canadian institutionsHospital for Sick ChildrenUniversity of Toronto
Fundersnot available
KeywordsAutophagyATG5IRS1PI3K/AKT/mTOR pathwayCell biologyInsulin-like growth factor 1 receptorProtein kinase BInsulin receptor substrateInsulin receptorBiologyInsulinGrowth factorInsulin-like growth factorChemistryPhosphorylationSignal transductionReceptorInsulin resistanceEndocrinologyBiochemistryApoptosis

Abstract

fetched live from OpenAlex

Autophagy is a degradation pathway persisting in all cells at basal levels and further activated by various stimuli, such as starvation. This cellular process is mediated by autophagy‐related (Atg) proteins, which govern cargo recognition and formation of a nascent organelle called the autophagosome. Several Atg proteins have been identified, including Atg3 and the Atg12‐Atg5‐Atg16L1 complex. Recently, connections between autophagy and insulin action have emerged. The insulin receptor (IR) and insulin‐like growth factor receptor (IGF1R) bind and phosphorylate insulin receptor substrate 1 (IRS1) leading to PI3K/Akt activation, which through downstream activation of mTORC1 inhibit autophagy. On the other hand, tissue‐specific, autophagy‐deficient mouse models have attenuated basal and insulin‐stimulated PI3K/Akt signalling. Similarly, expression of the dominant‐negative mutant ATG5K130R in L6 myoblasts reduces insulin‐induced Akt and IRS1 phosphorylation. As growth factor signalling reduces autophagy, these findings suggest a potential feedback mechanism whereby deficient autophagy acts to attenuate insulin signalling. However, the mechanism through which reduced autophagy feeds back onto insulin signalling remains unknown. We hypothesize that interfering with autophagy affects insulin and IGF1 signalling at different levels, including IR, IGF1R and IRS1, and we investigate the potential underlying mechanism. To examine the interplay between deficient autophagy and insulin action, we treated mouse embryonic fibroblasts (MEFs) depleted of Atg3, Atg5, Atg12 or Atg16L1 with 10nM insulin or 100ng/ml (13.3nM) IGF1. Atg depletion did not induce changes in IR content, its localization at the plasma membrane or insulin binding. Interestingly, Atg16L1‐KO MEFs have reduced IRS1 and IRS2 protein content and gene expression, which suggests that defective Atg16L1 affects IRS gene transcription. ER stress is known to reduce Foxo1 protein content, an important transcription factor of IRS, and we have found elevated ER stress in Atg16L1‐KO MEFs. Accordingly, Atg16L1‐ and Atg5‐KO MEFs exhibited attenuated insulin‐ and IGF1‐induced Akt phosphorylation at both S473 and T308 compared to WT. In contrast, insulin‐ and IGF1‐induced Akt phosphorylation was inhibited selectively at T308 in Atg3‐KO MEFs, and at S473 in Atg12 KO MEFs. In conclusion, Atg16L1 appears to induce insulin and IGF1 resistance through decreased IRS1 and IRS2 expression, while Atg3 Atg5 and Atg12 affect signalling at the level of Akt. Support or Funding Information SFC is funded by NSERC‐CGS. This abstract is from the Experimental Biology 2018 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)0.0010.001
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 head0.019
GPT teacher head0.280
Teacher spread0.262 · 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
Published2018
Admission routes1
Has abstractyes

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