Evidence map›Paper›PMID 34285405›Full record

ReviewNature reviews. Molecular cell biology2021

The aetiology and molecular landscape of insulin resistance.

David E James, Jacqueline Stöckli, Morris J Birnbaum

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07284316 (Effect of a Multidomain Intervention Plus Turmeric on the Prevention of Cognitive Decline in People Over 55 Years of Age With Insulin Resistance), which is not on this map. Cited by 360 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
360citing papers in PubMed, 6 pooled it
34.3field-weighted citation impact, top 1% 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.

NCT07284316 phase2 / phase3active not recruitingnot on this mapstarted 2025, after this paper: background citation

Effect of a Multidomain Intervention Plus Turmeric on the Prevention of Cognitive Decline in People Over 55 Years of Age With Insulin Resistance: A Randomized Clinical Trial

TypeinterventionalSponsorInstituto Mexicano del Seguro SocialRan2025 to 2027Enrolled100ConditionsCognitive Decline, Subjective Cognitive Impairment, Insulin ResistanceArmsTurmeric extract, Control: Placebo. 500mg gelatin in capsules 2 times a day
3 · Its place in the literature

Who cites it

360 citing papers in PubMed, 6 syntheses or guidelines pooled it, 624 citations in OpenAlex.

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300 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

David E JamesCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia. david.james@sydney.edu.au.ORCID http://orcid.org/0000-0001-5946-5257
Jacqueline StöckliCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-6446-7350
Morris J BirnbaumInternal Medicine Research Unit, Pfizer Inc., Cambridge, MA, USA. Morris.Birnbaum@pfizer.com.ORCID http://orcid.org/0000-0001-9972-8680
The University of Sydney · AUPfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance, defined as a defect in insulin-mediated control of glucose metabolism in tissues - prominently in muscle, fat and liver - is one of the earliest manifestations of a constellation of human diseases that includes type 2 diabetes and cardiovascular disease. These diseases are typically associated with intertwined metabolic abnormalities, including obesity, hyperinsulinaemia, hyperglycaemia and hyperlipidaemia. Insulin resistance is caused by a combination of genetic and environmental factors. Recent genetic and biochemical studies suggest a key role for adipose tissue in the development of insulin resistance, potentially by releasing lipids and other circulating factors that promote insulin resistance in other organs. These extracellular factors perturb the intracellular concentration of a range of intermediates, including ceramide and other lipids, leading to defects in responsiveness of cells to insulin. Such intermediates may cause insulin resistance by inhibiting one or more of the proximal components in the signalling cascade downstream of insulin (insulin receptor, insulin receptor substrate (IRS) proteins or AKT). However, there is now evidence to support the view that insulin resistance is a heterogeneous disorder that may variably arise in a range of metabolic tissues and that the mechanism for this effect likely involves a unified insulin resistance pathway that affects a distal step in the insulin action pathway that is more closely linked to the terminal biological response. Identifying these targets is of major importance, as it will reveal potential new targets for treatments of diseases associated with insulin resistance.

Indexed as

Antigens, CDDiabetes Mellitus, Type 2GlucoseHumansInsulinInsulin ResistanceLiverMuscle, SkeletalObesityProto-Oncogene Proteins c-aktReceptor, InsulinSignal TransductionAntigens, CDGlucoseINSR protein, humanInsulinProto-Oncogene Proteins c-aktReceptor, Insulin

Identifiers

PMID34285405
OpenAlexW3184395450

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.