| IL-6 deficiency in mice neither impairs induction of metabolic genes in the liver nor affects blood glucose levels during fasting and moderately intense exercise. | |
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MedLine Citation:
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PMID: 20411234 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS/HYPOTHESIS: Fasting and exercise are strong physiological stimuli for hepatic glucose production. IL-6 has been implicated in the regulation of gluconeogenic genes, but the results are contradictory and the relevance of IL-6 for fasting- and exercise-induced hepatic glucose production is not clear. METHODS: Investigations were performed in rat hepatoma cells, and on C57Bl6 and Il6(-/-) mice under the following conditions: IL-6 stimulation/injection, non-exhaustive exercise (60 min run on a treadmill) and fasting for 16 h. Metabolite analysis, quantitative real-time PCR and immunoblotting were performed. RESULTS: IL-6 stimulation of rat hepatoma cells led to higher glucose production. Injection of IL-6 in mice slightly increased hepatic Pepck (also known as Pck1) expression. Fasting of Il6(-/-) mice for 16 h did not alter glucose production compared with wild-type mice, since plasma glucose concentrations were similar and upregulation of phosphoenolpyruvate carboxykinase (PEPCK) and Pgc-1alpha (also known as Ppargc1a) expression was comparable. In the non-fasting state, Il6(-/-) mice showed a mild metabolic alteration including higher plasma glucose and insulin levels, lower NEFA concentrations and slightly increased hepatic PEPCK content. Moderately intense exercise resulted in elevated IL-6 plasma levels in wild-type mice. Despite that, plasma glucose, insulin, NEFA levels and hepatic glycogen content were not different in Il6(-/-) mice immediately after running, while expression of hepatic G6pc, Pgc-1alpha, Irs2 and Igfbp1 mRNA was similarly increased. CONCLUSIONS/INTERPRETATION: These data suggest that in mice IL-6 is not essential for physiologically increased glucose production during fasting or non-exhaustive exercise. |
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Authors:
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L Fritsche; M Hoene; R Lehmann; H Ellingsgaard; A M Hennige; A K Pohl; H U Häring; E D Schleicher; C Weigert |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-22 |
Journal Detail:
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Title: Diabetologia Volume: 53 ISSN: 1432-0428 ISO Abbreviation: Diabetologia Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-06-25 Completed Date: 2010-09-27 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0006777 Medline TA: Diabetologia Country: Germany |
Other Details:
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Languages: eng Pagination: 1732-42 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, Division of Pathobiochemistry and Clinical Chemistry, University of Tuebingen, Otfried-Mueller-Strasse 10, 72076 Tuebingen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Glucose / genetics, metabolism* Blotting, Western Cells, Cultured Fasting / metabolism* Gene Expression / drug effects, physiology Gluconeogenesis / genetics Glycogen / genetics, metabolism Insulin / genetics, metabolism Interleukin-6 / genetics, metabolism*, pharmacology Liver / cytology, drug effects, metabolism* Mice Mice, Knockout Phosphoenolpyruvate Carboxykinase (ATP) / genetics, metabolism Physical Conditioning, Animal / physiology* RNA, Messenger / genetics, metabolism Rats |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Interleukin-6; 0/RNA, Messenger; 11061-68-0/Insulin; 9005-79-2/Glycogen; EC 4.1.1.49/Phosphoenolpyruvate Carboxykinase (ATP) |
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