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Interleukin-6-defic...
Interleukin-6-deficient mice develop hepatic inflammation and systemic insulin resistance.
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Matthews, V B (författare)
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Allen, T L (författare)
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Risis, S (författare)
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visa fler...
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Chan, M H S (författare)
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Henstridge, D C (författare)
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Watson, N (författare)
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Zaffino, L A (författare)
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Babb, J R (författare)
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Boon, J (författare)
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Meikle, P J (författare)
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Jowett, J B (författare)
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Watt, M J (författare)
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- Jansson, John-Olov, 1954 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
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Bruce, C R (författare)
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Febbraio, M A (författare)
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(creator_code:org_t)
- 2010-08-11
- 2010
- Engelska.
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 53:11, s. 2431-2441
- Relaterad länk:
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https://gup.ub.gu.se...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- Cytokines
- Fatty liver
- Obesity
- Signal transduction
- Type 2 diabetes
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Till lärosätets databas
- Av författaren/redakt...
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Matthews, V B
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Allen, T L
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Risis, S
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Chan, M H S
-
Henstridge, D C
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Watson, N
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visa fler...
-
Zaffino, L A
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Babb, J R
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Boon, J
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Meikle, P J
-
Jowett, J B
-
Watt, M J
-
Jansson, John-Ol ...
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Bruce, C R
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Febbraio, M A
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visa färre...
- Artiklar i publikationen
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Diabetologia
- Av lärosätet
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Göteborgs universitet