Evidence map›Paper›PMID 34720091›Full record

ArticleThe Journal of clinical investigation2021

Deprogram and reprogram to solve the riddle of insulin resistance.

Victoria L Tokarz, Paul Delgado-Olguín, Amira Klip

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Victoria L TokarzCell Biology Program, The Hospital for Sick Children, Toronto, Canada.
Paul Delgado-OlguínTranslational Medicine Program, The Hospital for Sick Children, Toronto, Canada.
Amira KlipCell Biology Program, The Hospital for Sick Children, Toronto, Canada.
University of Toronto · CA

Funding

CIHR 149046CIHR 162208CIHR FDN-143203
6 · The paper itself

Abstract

Skeletal muscle preeminently determines whole-body glycemia. However, the molecular basis and inheritable influence that drive the progression of insulin resistance to type 2 diabetes remain debated. In this issue of the JCI, Haider and Lebastchi report on their use of induced pluripotent stem cell-derived (iPSC-derived) myoblasts (iMyos) to uncover multiple phosphoproteomic changes that carried over from the human to the cell-culture system. In this system devoid of in vivo influences, the researchers annotated changes between the sexes and between the most and least insulin-sensitive quintiles of a healthy population (defined by steady-state blood glucose levels). Many phosphoproteomic differences were detected in the absence of insulin, revealing that changes in the basal landscape of cells determine the efficiency of insulin action. Basal and insulin-dependent deficiencies of iPSCs and iMyos likely involve genetic and epigenetic determinants that modulate insulin sensitivity.

Indexed as

Diabetes Mellitus, Type 2Induced Pluripotent Stem CellsInsulin ResistanceBlood GlucoseHumansInsulinMuscle, SkeletalBlood GlucoseInsulin

Identifiers

PMID34720091
PMCPMC8553549
OpenAlexW3211329272

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.