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Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise

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Standard

Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise. / Bertholdt, Lærke; Gudiksen, Anders; Schwartz, Camilla Lindgren; Knudsen, Jakob Grunnet; Pilegaard, Henriette.

I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Bind 312, Nr. 4, 07.04.2017, s. R626-R636.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Bertholdt, L, Gudiksen, A, Schwartz, CL, Knudsen, JG & Pilegaard, H 2017, 'Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise', American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, bind 312, nr. 4, s. R626-R636. https://doi.org/10.1152/ajpregu.00373.2016

APA

Bertholdt, L., Gudiksen, A., Schwartz, C. L., Knudsen, J. G., & Pilegaard, H. (2017). Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 312(4), R626-R636. https://doi.org/10.1152/ajpregu.00373.2016

Vancouver

Bertholdt L, Gudiksen A, Schwartz CL, Knudsen JG, Pilegaard H. Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2017 apr 7;312(4):R626-R636. https://doi.org/10.1152/ajpregu.00373.2016

Author

Bertholdt, Lærke ; Gudiksen, Anders ; Schwartz, Camilla Lindgren ; Knudsen, Jakob Grunnet ; Pilegaard, Henriette. / Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise. I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2017 ; Bind 312, Nr. 4. s. R626-R636.

Bibtex

@article{b038d6c109be4a8f926f8eedea618710,
title = "Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise",
abstract = "The liver is essential in maintaining and regulating glucose homeostasis during prolonged exercise. IL-6 has been shown to be secreted from skeletal muscle during exercise and has been suggested to signal to the liver. Therefore, the aim of this study was to investigate the role of skeletal muscle IL-6 on hepatic glucose regulation and substrate choice during prolonged exercise. Skeletal muscle-specific IL-6 knockout (IL-6 MKO) mice (age, 12-14 wk) and littermate lox/lox (Control) mice were either rested (Rest) or completed a single bout of exercise for 10, 60, or 120 min, and the liver was quickly obtained. Hepatic IL-6 mRNA was higher at 60 min of exercise, and hepatic signal transducer and activator of transcription 3 was higher at 120 min of exercise than at rest in both genotypes. Hepatic glycogen was higher in IL-6 MKO mice than control mice at rest, but decreased similarly during exercise in the two genotypes, and hepatic glucose content was lower in IL-6 MKO than control mice at 120 min of exercise. Hepatic phosphoenolpyruvate carboxykinase mRNA and protein increased in both genotypes at 120 min of exercise, whereas hepatic glucose 6 phosphatase protein remained unchanged. Furthermore, IL-6 MKO mice had higher hepatic pyruvate dehydrogenase (PDH)Ser232 and PDHSer300 phosphorylation than control mice at rest. In conclusion, hepatic gluconeogenic capacity in mice is increased during prolonged exercise independent of muscle IL-6. Furthermore, Skeletal muscle IL-6 influences hepatic substrate regulation at rest and hepatic glucose metabolism during prolonged exercise, seemingly independent of IL-6 signaling in the liver.",
keywords = "Exercise, Glucose metabolism, IL-6, Liver, Skeletal muscle, Substrate choice",
author = "L{\ae}rke Bertholdt and Anders Gudiksen and Schwartz, {Camilla Lindgren} and Knudsen, {Jakob Grunnet} and Henriette Pilegaard",
year = "2017",
month = apr,
day = "7",
doi = "10.1152/ajpregu.00373.2016",
language = "English",
volume = "312",
pages = "R626--R636",
journal = "American Journal of Physiology: Regulatory, Integrative and Comparative Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "4",

}

RIS

TY - JOUR

T1 - Lack of skeletal muscle IL-6 influences hepatic glucose metabolism in mice during prolonged exercise

AU - Bertholdt, Lærke

AU - Gudiksen, Anders

AU - Schwartz, Camilla Lindgren

AU - Knudsen, Jakob Grunnet

AU - Pilegaard, Henriette

PY - 2017/4/7

Y1 - 2017/4/7

N2 - The liver is essential in maintaining and regulating glucose homeostasis during prolonged exercise. IL-6 has been shown to be secreted from skeletal muscle during exercise and has been suggested to signal to the liver. Therefore, the aim of this study was to investigate the role of skeletal muscle IL-6 on hepatic glucose regulation and substrate choice during prolonged exercise. Skeletal muscle-specific IL-6 knockout (IL-6 MKO) mice (age, 12-14 wk) and littermate lox/lox (Control) mice were either rested (Rest) or completed a single bout of exercise for 10, 60, or 120 min, and the liver was quickly obtained. Hepatic IL-6 mRNA was higher at 60 min of exercise, and hepatic signal transducer and activator of transcription 3 was higher at 120 min of exercise than at rest in both genotypes. Hepatic glycogen was higher in IL-6 MKO mice than control mice at rest, but decreased similarly during exercise in the two genotypes, and hepatic glucose content was lower in IL-6 MKO than control mice at 120 min of exercise. Hepatic phosphoenolpyruvate carboxykinase mRNA and protein increased in both genotypes at 120 min of exercise, whereas hepatic glucose 6 phosphatase protein remained unchanged. Furthermore, IL-6 MKO mice had higher hepatic pyruvate dehydrogenase (PDH)Ser232 and PDHSer300 phosphorylation than control mice at rest. In conclusion, hepatic gluconeogenic capacity in mice is increased during prolonged exercise independent of muscle IL-6. Furthermore, Skeletal muscle IL-6 influences hepatic substrate regulation at rest and hepatic glucose metabolism during prolonged exercise, seemingly independent of IL-6 signaling in the liver.

AB - The liver is essential in maintaining and regulating glucose homeostasis during prolonged exercise. IL-6 has been shown to be secreted from skeletal muscle during exercise and has been suggested to signal to the liver. Therefore, the aim of this study was to investigate the role of skeletal muscle IL-6 on hepatic glucose regulation and substrate choice during prolonged exercise. Skeletal muscle-specific IL-6 knockout (IL-6 MKO) mice (age, 12-14 wk) and littermate lox/lox (Control) mice were either rested (Rest) or completed a single bout of exercise for 10, 60, or 120 min, and the liver was quickly obtained. Hepatic IL-6 mRNA was higher at 60 min of exercise, and hepatic signal transducer and activator of transcription 3 was higher at 120 min of exercise than at rest in both genotypes. Hepatic glycogen was higher in IL-6 MKO mice than control mice at rest, but decreased similarly during exercise in the two genotypes, and hepatic glucose content was lower in IL-6 MKO than control mice at 120 min of exercise. Hepatic phosphoenolpyruvate carboxykinase mRNA and protein increased in both genotypes at 120 min of exercise, whereas hepatic glucose 6 phosphatase protein remained unchanged. Furthermore, IL-6 MKO mice had higher hepatic pyruvate dehydrogenase (PDH)Ser232 and PDHSer300 phosphorylation than control mice at rest. In conclusion, hepatic gluconeogenic capacity in mice is increased during prolonged exercise independent of muscle IL-6. Furthermore, Skeletal muscle IL-6 influences hepatic substrate regulation at rest and hepatic glucose metabolism during prolonged exercise, seemingly independent of IL-6 signaling in the liver.

KW - Exercise

KW - Glucose metabolism

KW - IL-6

KW - Liver

KW - Skeletal muscle

KW - Substrate choice

UR - http://www.scopus.com/inward/record.url?scp=85017288561&partnerID=8YFLogxK

U2 - 10.1152/ajpregu.00373.2016

DO - 10.1152/ajpregu.00373.2016

M3 - Journal article

C2 - 28122718

AN - SCOPUS:85017288561

VL - 312

SP - R626-R636

JO - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

JF - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

SN - 0363-6119

IS - 4

ER -

ID: 181451461