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Sachs, S. ; Zarini, S.* ; Kahn, D.E.* ; Harrison, K.A.* ; Perreault, L.* ; Phang, T.* ; Newsom, S.A.* ; Strauss, A.* ; Kerege, A.* ; Schoen, J.A.* ; Bessesen, D.H.* ; Schwarzmayr, T. ; Graf, E. ; Lutter, D. ; Krumsiek, J. ; Hofmann, S.M. ; Bergman, B.C.*

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

Am. J. Physiol. Endocrinol. Metab. 316, E866-E879 (2019)
Verlagsversion Postprint DOI PMC
Open Access Gold
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 unoaver 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adipose Tissue Distribution ; Emcl ; Insulin Sensitivity ; Myosteatosis; Extracellular-matrix; Glucose-tolerance; Body-fat; Men; Obesity; Infiltration; Association; Lipolysis; Suppression; Reductions
Sprache englisch
Veröffentlichungsjahr 2019
HGF-Berichtsjahr 2019
ISSN (print) / ISBN 0193-1849
e-ISSN 1522-1555
Zeitschrift American Journal of Physiology - Endocrinology and Metabolism
Quellenangaben Band: 316, Heft: 5, Seiten: E866-E879 Artikelnummer: , Supplement: ,
Verlag American Physiological Society
Verlagsort 9650 Rockville Pike, Bethesda, Md 20814 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
Institute of Human Genetics (IHG)
Institute of Diabetes and Obesity (IDO)
Institute of Computational Biology (ICB)
POF Topic(s) 30201 - Metabolic Health
30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
30205 - Bioengineering and Digital Health
Forschungsfeld(er) Helmholtz Diabetes Center
Genetics and Epidemiology
Enabling and Novel Technologies
PSP-Element(e) G-502390-001
G-500700-001
G-502297-001
G-554100-001
G-502200-001
DOI 10.1152/ajpendo.00243.2018
WOS ID WOS:000467084600016
Scopus ID 85065313868
PubMed ID 30620635
Erfassungsdatum 2019-03-01
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