Evidence map›Paper›PMID 30620635›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2019

Intermuscular adipose tissue directly modulates skeletal muscle insulin sensitivity in humans.

Stephan Sachs, Simona Zarini, Darcy E Kahn, Kathleen A Harrison, Leigh Perreault, Tzu Phang, Sean A Newsom, Allison Strauss, Anna Kerege, Jonathan A Schoen and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 3 pooled it
10.3field-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.

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

125 citing papers in PubMed, 3 syntheses or guidelines pooled it, 177 citations in OpenAlex.

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65 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

17 authors at 5 institutions in 2 countries.

Stephan SachsInstitute for Diabetes and Regeneration, Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany.
Simona ZariniUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Darcy E KahnUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Kathleen A HarrisonUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Leigh PerreaultUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Tzu PhangUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Sean A NewsomOregon State University , Corvallis, Oregon.
Allison StraussUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Anna KeregeUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Jonathan A SchoenUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Daniel H BessesenUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
Thomas SchwarzmayrInstitute of Human Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany.
Elisabeth GrafInstitute of Human Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany.
Dominik LutterInstitute for Diabetes and Obesity, Helmholtz Diabetes Center at Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany.
Jan KrumsiekInstitute of Computational Biology, Helmholtz Zentrum München, Neuherberg, Germany and German Center for Diabetes Research (DZD) , Neuherberg , Germany.
Susanna M HofmannInstitute for Diabetes and Regeneration, Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany.
Bryan C BergmanUniversity of Colorado Anschutz Medical Campus , Aurora, Colorado.
University of Colorado Anschutz Medical Campus · USHelmholtz Zentrum München · DEHeinrich Heine University Düsseldorf · DEGerman Center for Diabetes Research · DEOregon State University · US

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Edward L Melanson · 1995 to 2026
$32.6M
NIDDK National Research Service Award (NRSA) T32 Diversity Administrative SupplementT32DK007658 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Kristen Elizabeth Boyle, Ihuoma U Eneli · 1991 to 2026
$6.0M
Intermuscular adipose tissue (IMAT): protagonist in sarcopenia and insulin resistance in humansR01DK118149 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BERGMAN, BRYAN C · 2018 to 2022
$2.9M
Localization of saturated diacylglycerol and insulin sensitivity in humansR01DK089170 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BERGMAN, BRYAN C · 2010 to 2014
$1.4M
NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK089170NIDDK NIH HHS R01 DK118149NIDDK NIH HHS T32 DK007658
6 · The paper itself

Abstract

Intermuscular adipose tissue (IMAT) is negatively related to insulin sensitivity, but a causal role of IMAT in the development of insulin resistance is unknown. IMAT was sampled in humans to test for the ability to induce insulin resistance in vitro and characterize gene expression to uncover how IMAT may promote skeletal muscle insulin resistance. Human primary muscle cells were incubated with conditioned media from IMAT, visceral (VAT), or subcutaneous adipose tissue (SAT) to evaluate changes in insulin sensitivity. RNAseq analysis was performed on IMAT with gene expression compared with skeletal muscle and SAT, and relationships to insulin sensitivity were determined in men and women spanning a wide range of insulin sensitivity measured by hyperinsulinemic-euglycemic clamp. Conditioned media from IMAT and VAT decreased insulin sensitivity similarly compared with SAT. Multidimensional scaling analysis revealed distinct gene expression patterns in IMAT compared with SAT and muscle. Pathway analysis revealed that IMAT expression of genes in insulin signaling, oxidative phosphorylation, and peroxisomal metabolism related positively to donor insulin sensitivity, whereas expression of macrophage markers, inflammatory cytokines, and secreted extracellular matrix proteins were negatively related to insulin sensitivity. Perilipin 5 gene expression suggested greater IMAT lipolysis in insulin-resistant individuals. Combined, these data show that factors secreted from IMAT modulate muscle insulin sensitivity, possibly via secretion of inflammatory cytokines and extracellular matrix proteins, and by increasing local FFA concentration in humans. These data suggest IMAT may be an important regulator of skeletal muscle insulin sensitivity and could be a novel therapeutic target for skeletal muscle insulin resistance.

Indexed as

Adipose TissueAdultAthletesDiabetes Mellitus, Type 2Fatty Acids, NonesterifiedFemaleGene Expression ProfilingGene Expression RegulationGlucose Clamp TechniqueHumansInsulin ResistanceIntra-Abdominal FatMaleMiddle AgedMuscle Fibers, SkeletalMuscle, SkeletalFatty Acids, Nonesterifiedadipose tissue distributionEMCLinsulin sensitivitymyosteatosis

Identifiers

PMID30620635
PMCPMC6580171
OpenAlexW2909780617

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.