Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle
Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle Stephan Glund 1 , Atul Deshmukh 1 , Yun Chau Long 1 , Theodore Moller 1 , Heikki A. Koistinen 2 , Kenneth Caidahl 3 , Juleen R. Zierath 1 and Anna Krook 1 4 1 Department of Molecular Medicine and Surgery, Section fo...
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Published in | Diabetes (New York, N.Y.) Vol. 56; no. 6; pp. 1630 - 1637 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.06.2007
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Subjects | |
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Abstract | Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle
Stephan Glund 1 ,
Atul Deshmukh 1 ,
Yun Chau Long 1 ,
Theodore Moller 1 ,
Heikki A. Koistinen 2 ,
Kenneth Caidahl 3 ,
Juleen R. Zierath 1 and
Anna Krook 1 4
1 Department of Molecular Medicine and Surgery, Section for Integrative Physiology, Karolinska University Hospital, Karolinska
Institutet, Stockholm, Sweden
2 Helsinki University Central Hospital and Biomedicum, Helsinki, Finland
3 Department of Molecular Medicine and Surgery, Section for Clinical Physiology, Karolinska University Hospital, Karolinska
Institutet, Stockholm, Sweden
4 Department of Physiology and Pharmacology, Section for Integrative Physiology, Karolinska Institutet, Stockholm, Sweden
Address correspondence and reprint requests to Anna Krook, Department of Physiology and Pharmacology, Section for Integrative
Physiology, Karolinska Institutet, von Eulers väg 4, SE-171 77 Stockholm, Sweden. E-mail: anna.krook{at}ki.se
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.
AMPK, AMP-activated protein kinase
AS160, Akt substrate of 160 kDa
GSK, glycogen synthase kinase
IL, interleukin
IRS, insulin receptor substrate
KHBB, Krebs-Henseleit bicarbonate buffer
MAPK, mitogen-activated protein kinase
PKB, protein kinase B
STAT, signal transducer and activator of transcription
Footnotes
Published ahead or print at http://diabetes.diabetesjournals.org on 15 March 2007. DOI: 10.2337/db06-1733.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted February 23, 2007.
Received December 13, 2006.
DIABETES |
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AbstractList | 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 GSK3alpha/beta (glycogen synthase kinase 3alpha/beta) 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. 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. 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 GSK3alpha/beta (glycogen synthase kinase 3alpha/beta) 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. 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 $6 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/beta]) 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. Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle Stephan Glund 1 , Atul Deshmukh 1 , Yun Chau Long 1 , Theodore Moller 1 , Heikki A. Koistinen 2 , Kenneth Caidahl 3 , Juleen R. Zierath 1 and Anna Krook 1 4 1 Department of Molecular Medicine and Surgery, Section for Integrative Physiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden 2 Helsinki University Central Hospital and Biomedicum, Helsinki, Finland 3 Department of Molecular Medicine and Surgery, Section for Clinical Physiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden 4 Department of Physiology and Pharmacology, Section for Integrative Physiology, Karolinska Institutet, Stockholm, Sweden Address correspondence and reprint requests to Anna Krook, Department of Physiology and Pharmacology, Section for Integrative Physiology, Karolinska Institutet, von Eulers väg 4, SE-171 77 Stockholm, Sweden. E-mail: anna.krook{at}ki.se 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. AMPK, AMP-activated protein kinase AS160, Akt substrate of 160 kDa GSK, glycogen synthase kinase IL, interleukin IRS, insulin receptor substrate KHBB, Krebs-Henseleit bicarbonate buffer MAPK, mitogen-activated protein kinase PKB, protein kinase B STAT, signal transducer and activator of transcription Footnotes Published ahead or print at http://diabetes.diabetesjournals.org on 15 March 2007. DOI: 10.2337/db06-1733. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted February 23, 2007. Received December 13, 2006. DIABETES 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 GSK3 alpha /{szligbeta} (glycogen synthase kinase 3 alpha /{szligbeta}) 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. |
Audience | Professional |
Author | Atul Deshmukh Juleen R. Zierath Stephan Glund Kenneth Caidahl Anna Krook Theodore Moller Yun Chau Long Heikki A. Koistinen |
Author_xml | – sequence: 1 givenname: Stephan surname: Glund fullname: Glund, Stephan organization: Department of Molecular Medicine and Surgery, Section for Integrative Physiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden – sequence: 2 givenname: Atul surname: Deshmukh fullname: Deshmukh, Atul – sequence: 3 givenname: Yun Chau surname: Long fullname: Long, Yun Chau – sequence: 4 givenname: Theodore surname: Moller fullname: Moller, Theodore – sequence: 5 givenname: Heikki A surname: Koistinen fullname: Koistinen, Heikki A – sequence: 6 givenname: Kenneth surname: Caidahl fullname: Caidahl, Kenneth – sequence: 7 givenname: Juleen R surname: Zierath fullname: Zierath, Juleen R – sequence: 8 givenname: Anna surname: Krook fullname: Krook, Anna |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18811670$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17363741$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/267982$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:115529383$$DView record from Swedish Publication Index |
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Copyright | 2007 INIST-CNRS COPYRIGHT 2007 American Diabetes Association Copyright American Diabetes Association Jun 2007 |
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Snippet | Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle
Stephan Glund 1 ,
Atul Deshmukh 1 ,
Yun Chau Long 1 ,
Theodore Moller 1 ,... Interleukin (IL)-6 is a proinflammatory cytokine shown to modify insulin sensitivity. Elevated plasma levels of IL-6 are observed in insulin-resistant states.... |
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SubjectTerms | Adipocytes Adult Biological and medical sciences Biological Transport - drug effects Biopsy Body fat Clinical Medicine Cytokines Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fundamental and applied biological sciences. Psychology Genetic Glucose Glucose - metabolism Glycogen - biosynthesis Humans Insulin resistance Interleukin-6 Interleukin-6 - genetics Interleukin-6 - pharmacology Interleukin-6/genetics/pharmacology Kinases Klinisk medicin Male Medical sciences Medicin och hälsovetenskap Metabolism Middle Aged Muscle Muscle, Skeletal - cytology Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Muscles Musculoskeletal system Obesity Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Plasma Polymorphism Polymorphism, Genetic Polymorphism, Restriction Fragment Length Proteins Reference Values Restriction Fragment Length Signal Transduction Skeletal muscle Skeletal/cytology/drug effects/metabolism Striated muscle. Tendons Tumor necrosis factor-TNF Vertebrates: osteoarticular system, musculoskeletal system |
Title | Interleukin-6 Directly Increases Glucose Metabolism in Resting Human Skeletal Muscle |
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