id:"swepub:oai:gup.ub.gu.se/126610"
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- Matthews, V B (author)
Interleukin-6-deficient mice develop hepatic inflammation and systemic insulin resistance.
- Article/chapterEnglish2010
Publisher, publication year, extent ...
- 2010-08-11
- Springer Science and Business Media LLC,2010
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- LIBRIS-ID:oai:gup.ub.gu.se/126610
- https://gup.ub.gu.se/publication/126610URI
- https://doi.org/10.1007/s00125-010-1865-yDOI
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- Language:English
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- SwePubSwePub
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- AIMS/HYPOTHESIS: The role of IL-6 in the development of obesity and hepatic insulin resistance is unclear and still the subject of controversy. We aimed to determine whether global deletion of Il6 in mice (Il6 (-/-)) results in standard chow-induced and high-fat diet (HFD)-induced obesity, hepatosteatosis, inflammation and insulin resistance. METHODS: Male, 8-week-old Il6 (-/-) and littermate control mice were fed a standard chow or HFD for 12 weeks and phenotyped accordingly. RESULTS: Il6 (-/-) mice displayed obesity, hepatosteatosis, liver inflammation and insulin resistance when compared with control mice on a standard chow diet. When fed a HFD, the Il6 (-/-) and control mice had marked, equivalent gains in body weight, fat mass and ectopic lipid deposition in the liver relative to chow-fed animals. Despite this normalisation, the greater liver inflammation, damage and insulin resistance observed in chow-fed Il6 (-/-) mice relative to control persisted when both were fed the HFD. Microarray analysis from livers of mice fed a HFD revealed that genes associated with oxidative phosphorylation, the electron transport chain and tricarboxylic acid cycle were uniformly decreased in Il6 (-/-) relative to control mice. This coincided with reduced maximal activity of the mitochondrial enzyme beta-hydroxyacyl-CoA-dehydrogenase and decreased levels of mitochondrial respiratory chain proteins. CONCLUSIONS/INTERPRETATION: Our data suggest that IL-6 deficiency exacerbates HFD-induced hepatic insulin resistance and inflammation, a process that appears to be related to defects in mitochondrial metabolism.
Subject headings and genre
- Cytokines
- Fatty liver
- Obesity
- Signal transduction
- Type 2 diabetes
Added entries (persons, corporate bodies, meetings, titles ...)
- Allen, T L (author)
- Risis, S (author)
- Chan, M H S (author)
- Henstridge, D C (author)
- Watson, N (author)
- Zaffino, L A (author)
- Babb, J R (author)
- Boon, J (author)
- Meikle, P J (author)
- Jowett, J B (author)
- Watt, M J (author)
- Jansson, John-Olov,1954Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology(Swepub:gu)xjanjo (author)
- Bruce, C R (author)
- Febbraio, M A (author)
- Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för fysiologi (creator_code:org_t)
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- In:Diabetologia: Springer Science and Business Media LLC53:11, s. 2431-24411432-04280012-186X
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- Zaffino, L A
- Babb, J R
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