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Cited by 219Metabolism, Diabetes, and CancerExercise and Physiological ResponsesAdipokines, Inflammation, and Metabolic Diseases

Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle

Glund, Stephan, Deshmukh, Atul, Long, Yun Chau, Moller, Theodore, Koistinen, Heikki A., Caidahl, Kenneth, Zierath, Juleen R., Krook, Anna·2007·Diabetes
DOI 10.2337/db06-1733
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Abstract

Interleukin (IL)-6 is a proinflammatory cytokine shown to modify insulin sensitivity. Elevated plasma levels of IL-6 are observed in insulin-resistant states. Interestingly, plasma IL-6 levels also increase during exercise, with skeletal muscle being the predominant source. Thus, IL-6 has also been suggested to promote insulin-mediated glucose utilization. In this study, we determined the direct effects of IL-6 on glucose transport and signal transduction in human skeletal muscle. Skeletal muscle strips were prepared from vastus lateralis biopsies obtained from 22 healthy men. Muscle strips were incubated with or without IL-6 (120 ng/ml). We found that IL-6 increased glucose transport in human skeletal muscle 1.3-fold (P < 0.05). A 30-min pre-exposure to IL-6 did not affect insulin-stimulated glucose transport. IL-6 also increased skeletal muscle glucose incorporation into glycogen, as well as glucose oxidation (1.5- and 1.3-fold, respectively; P < 0.05). IL-6 increased phosphorylation of STAT3 (signal transducer and activator of transcription 3; P < 0.05), AMP-activated protein kinase (P = 0.063), and p38 mitogen-activated protein kinase (P < 0.05) and reduced phosphorylation of S6 ribosomal protein (P < 0.05). In contrast, phosphorylation of protein kinase B/Akt, AS160 (Akt substrate of 160 kDa), and GSK3α/β (glycogen synthase kinase 3α/β) as well as insulin receptor substrate 1–associated phosphatidylinositol 3-kinase activity remained unaltered. In conclusion, acute IL-6 exposure increases glucose metabolism in resting human skeletal muscle. Insulin-stimulated glucose transport and insulin signaling were unchanged after IL-6 exposure.

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Crossref · 10.2337/db06-1733

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Authors
Glund, S., Deshmukh, A., Long, Y. C., Moller, T., Koistinen, H. A., Caidahl, K., Zierath, J. R., & Krook, A.
Affiliations
  • Karolinska University Hospital (SE)
  • Helsinki University Hospital (FI)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2007-06-01
Volume
56
Issue
6
Pages
1630-1637
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/db06-1733
OpenAlex
W1980733995
Cited by
219
References
81
Citations by year
2026: 7 · 2025: 12 · 2024: 10 · 2023: 7 · 2022: 13 · 2021: 16 · 2020: 5 · 2019: 13 · 2018: 7 · 2017: 13 · 2016: 6 · 2015: 8 · 2014: 12 · 2013: 10 · 2012: 15
FWCI
6.49
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
interleukin-6, skeletal muscle glucose metabolism, glucose transport, insulin signaling, STAT3 phosphorylation, AMPK, p38 MAPK, ribosomal protein S6, glycogen synthesis, glucose oxidation, insulin resistance, inflammatory cytokines, vastus lateralis
MeSH terms
Adult, Biological Transport, Biopsy, Glucose, Glycogen, Humans, Male, Middle Aged, Polymorphism, Genetic, Reference Values, Polymorphism, Restriction Fragment Length, Signal Transduction, Interleukin-6, Muscle, Skeletal, Phosphatidylinositol 3-Kinases

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