Evidence map›Paper›PMID 30054342›Full record

ReviewJournal of lipid research2019

Muscle and adipose tissue insulin resistance: malady without mechanism?

Daniel J Fazakerley, James R Krycer, Alison L Kearney, Samantha L Hocking, David E James

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of lipid research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.

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34 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

5 authors at 1 institution in 1 country.

Daniel J FazakerleySchool of Life and Environmental Sciences, Central Clinical School, University of Sydney, Camperdown, New South Wales, Australia.ORCID http://orcid.org/0000-0001-8241-2903
James R KrycerSchool of Life and Environmental Sciences, Central Clinical School, University of Sydney, Camperdown, New South Wales, Australia.ORCID http://orcid.org/0000-0003-1536-7270
Alison L KearneySchool of Life and Environmental Sciences, Central Clinical School, University of Sydney, Camperdown, New South Wales, Australia.
Samantha L HockingFaculty of Medicine and Health, University of Sydney, Camperdown, New South Wales, Australia.
David E JamesSchool of Life and Environmental Sciences, Central Clinical School, University of Sydney, Camperdown, New South Wales, Australia david.james@sydney.edu.au.
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is a major risk factor for numerous diseases, including type 2 diabetes and cardiovascular disease. These disorders have dramatically increased in incidence with modern life, suggesting that excess nutrients and obesity are major causes of "common" insulin resistance. Despite considerable effort, the mechanisms that contribute to common insulin resistance are not resolved. There is universal agreement that extracellular perturbations, such as nutrient excess, hyperinsulinemia, glucocorticoids, or inflammation, trigger intracellular stress in key metabolic target tissues, such as muscle and adipose tissue, and this impairs the ability of insulin to initiate its normal metabolic actions in these cells. Here, we present evidence that the impairment in insulin action is independent of proximal elements of the insulin signaling pathway and is likely specific to the glucoregulatory branch of insulin signaling. We propose that many intracellular stress pathways act in concert to increase mitochondrial reactive oxygen species to trigger insulin resistance. We speculate that this may be a physiological pathway to conserve glucose during specific states, such as fasting, and that, in the presence of chronic nutrient excess, this pathway ultimately leads to disease. This review highlights key points in this pathway that require further research effort.

Indexed as

Insulin ResistanceAdipose TissueAnimalsBiological TransportGlucoseHumansMusclesGlucoseglucose transporter type 4insulin signalingmitochondriaoxidants

Identifiers

PMID30054342
PMCPMC6795081
OpenAlexW2883208799

What Socratic 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 Socratic graph.