Evidence map›Paper›PMID 24451368›Full record

ArticleThe Journal of biological chemistry2014

Myostatin induces insulin resistance via Casitas B-lineage lymphoma b (Cblb)-mediated degradation of insulin receptor substrate 1 (IRS1) protein in response to high calorie diet intake.

Sabeera Bonala, Sudarsanareddy Lokireddy, Craig McFarlane, Sreekanth Patnam, Mridula Sharma, Ravi Kambadur

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 53 citations in OpenAlex.

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  18. Does myostatin induce insulin resistance?The Journal of biological chemistry · 2014
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Sabeera BonalaFrom the School of Biological Sciences, Nanyang Technological University, Singapore 637551.
Sudarsanareddy Lokireddy
Craig McFarlane
Sreekanth Patnam
Mridula Sharma
Ravi Kambadur
Agency for Science, Technology and Research · SGNanyang Technological University · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To date a plethora of evidence has clearly demonstrated that continued high calorie intake leads to insulin resistance and type-2 diabetes with or without obesity. However, the necessary signals that initiate insulin resistance during high calorie intake remain largely unknown. Our results here show that in response to a regimen of high fat or high glucose diets, Mstn levels were induced in muscle and liver of mice. High glucose- or fat-mediated induction of Mstn was controlled at the level of transcription, as highly conserved carbohydrate response and sterol-responsive (E-box) elements were present in the Mstn promoter and were revealed to be critical for ChREBP (carbohydrate-responsive element-binding protein) or SREBP1c (sterol regulatory element-binding protein 1c) regulation of Mstn expression. Further molecular analysis suggested that the increased Mstn levels (due to high glucose or fatty acid loading) resulted in increased expression of Cblb in a Smad3-dependent manner. Casitas B-lineage lymphoma b (Cblb) is an ubiquitin E3 ligase that has been shown to specifically degrade insulin receptor substrate 1 (IRS1) protein. Consistent with this, our results revealed that elevated Mstn levels specifically up-regulated Cblb, resulting in enhanced ubiquitin proteasome-mediated degradation of IRS1. In addition, over expression or knock down of Cblb had a major impact on IRS1 and pAkt levels in the presence or absence of insulin. Collectively, these observations strongly suggest that increased glucose levels and high fat diet, both, result in increased circulatory Mstn levels. The increased Mstn in turn is a potent inducer of insulin resistance by degrading IRS1 protein via the E3 ligase, Cblb, in a Smad3-dependent manner.

Indexed as

Insulin ResistanceAnimalsBase SequenceBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseDiabetes Mellitus, Type 2DietDietary FatsGene Expression RegulationGlucoseHep G2 CellsHumansInsulin Receptor Substrate ProteinsLentivirusMiceMice, Inbred C57BLBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseCbl protein, mouseDietary FatsGlucoseInsulin Receptor Substrate ProteinsIrs1 protein, mouseMlxipl protein, mouseMyostatinNuclear ProteinsPalmitatesProto-Oncogene Proteins c-cblSmad3 ProteinSmad3 protein, mouseSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1Transcription FactorsCblbDiabetesHigh Fat DietHigh GlucoseInsulin ResistanceIRS1MyostatinSignalingSkeletal MuscleSkeletal Muscle Metabolism

Identifiers

PMID24451368
PMCPMC3953277
OpenAlexW2152737287

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.