Evidence map›Paper›PMID 26052434›Full record

ArticleInternational journal of obesity supplements2012

High-fat load: mechanism(s) of insulin resistance in skeletal muscle.

D S Lark, K H Fisher-Wellman, P D Neufer

Open access · greenAbstract read
In one paragraph

Article in International journal of obesity supplements, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.2field-weighted citation impact, top 45% 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, 40 citations in OpenAlex.

  1. Paternal obesity decreases infant MSC mitochondrial functional capacity.American journal of physiology. Endocrinology and metabolism · 2024
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  14. EXCLI journal · 2019
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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

3 authors at 1 institution in 1 country.

D S LarkEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA ; Department of Kinesiology, East Carolina University, Greenville, NC, USA.
K H Fisher-WellmanEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA ; Department of Kinesiology, East Carolina University, Greenville, NC, USA.
P D NeuferEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA ; Department of Kinesiology, East Carolina University, Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
East Carolina University · US

Funding

Linking Mitochondrial Bioenergetics to Muscle Insulin SensitivityR01DK074825 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2009 to 2013
$1.6M
Mitochondrial Bioenergetics and Etiology of Insulin ResistanceR01DK073488 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2007 to 2010
$1.2M
NIDDK NIH HHS R01 DK073488NIDDK NIH HHS R01 DK074825
6 · The paper itself

Abstract

Skeletal muscle from sedentary obese patients is characterized by depressed electron transport activity, reduced expression of genes required for oxidative metabolism, altered mitochondrial morphology and lower overall mitochondrial content. These findings imply that obesity, or more likely the metabolic imbalance that causes obesity, leads to a progressive decline in mitochondrial function, eventually culminating in mitochondrial dissolution or mitoptosis. A decrease in the sensitivity of skeletal muscle to insulin represents one of the earliest maladies associated with high dietary fat intake and weight gain. Considerable evidence has accumulated to suggest that the cytosolic ectopic accumulation of fatty acid metabolites, including diacylglycerol and ceramides, underlies the development of insulin resistance in skeletal muscle. However, an alternative mechanism has recently been evolving, which places the etiology of insulin resistance in the context of cellular/mitochondrial bioenergetics and redox systems biology. Overnutrition, particularly from high-fat diets, generates fuel overload within the mitochondria, resulting in the accumulation of partially oxidized acylcarnitines, increased mitochondrial hydrogen peroxide (H

Indexed as

H2O2 emissionhexokinaseinflammationintramyocellular fatmitochondriaredox environment

Identifiers

PMID26052434
PMCPMC4457392
OpenAlexW1997712034

What OpenQuestion holds

Textmetadata
LicenceTDM
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.