Evidence map›Paper›PMID 29847447›Full record

ReviewCurrent opinion in clinical nutrition and metabolic care2018

The manifold role of the mitochondria in skeletal muscle insulin resistance.

William Todd Cade

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in clinical nutrition and metabolic care, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

William Todd CadeProgram in Physical Therapy & Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Washington University in St. Louis · US

Funding

WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
Washington University Institute of Clinical and Translational Sciences (UL1)UL1RR024992 · NCRR · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2007 to 2011
$45.4M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
Heart and Skeletal Muscle Metabolism, Energetics and Function in Barth SyndromeR01HL107406 · NHLBI · WASHINGTON UNIVERSITY · PI CADE, WILLIAM TODD · 2012 to 2016
$2.2M
NCATS NIH HHS UL1 TR002345NCRR NIH HHS UL1 RR024992NHLBI NIH HHS R01 HL107406NIDDK NIH HHS P30 DK056341
6 · The paper itself

Abstract

purpose of reviewThe role of mitochondria in the development of skeletal muscle insulin resistance has been an area of intense investigation and debate for over 20 years. The mitochondria is a multifaceted organelle that plays an integral part in substrate metabolism and cellular signalling. This article aims to summarize the current findings and thought regarding the relationship between mitochondria and insulin resistance in skeletal muscle. RECENT

findingsSkeletal muscle insulin resistance was earlier thought to result from deficiency in mitochondrial oxidative capacity and ectopic lipid accumulation. Recent evidence suggests that skeletal muscle insulin resistance in high-energy intake models (i.e. obesity) results primarily from disrupted mitochondrial bioenergetics and alterations in mitochondrial-associated cell signalling. These signalling pathways include reactive oxygen species and redox balance, fatty acid β-oxidation intermediates, mitochondrial derived peptides, sirtuins, microRNAs and novel nuclear-encoded, mitochondria-acting peptides. SUMMARY: The pathophysiology of skeletal muscle insulin resistance is likely multifactorial involving many coordinated physiological processes. However, it is apparent that the mitochondria play an essential role in skeletal muscle insulin sensitivity in health, ageing and in numerous metabolic diseases. Deciphering the manifold functions of the mitochondria will allow us to understand the complex relationship between mitochondria and skeletal muscle insulin resistance.

Indexed as

Energy MetabolismInsulin ResistanceAnimalsFatty AcidsHumansInsulinMicroRNAsMitochondriaMuscle, SkeletalObesityPeptidesReactive Oxygen SpeciesSirtuinsFatty AcidsInsulinMicroRNAsPeptidesReactive Oxygen SpeciesSirtuins

Identifiers

PMID29847447
PMCPMC7001775
OpenAlexW2805895816

What OpenQuestion holds

Textmetadata
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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.