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Interleukin-6-deficient mice develop hepatic inflammation and systemic insulin resistance.

Artikel i vetenskaplig tidskrift
Författare V B Matthews
T L Allen
S Risis
M H S Chan
D C Henstridge
N Watson
L A Zaffino
J R Babb
J Boon
P J Meikle
J B Jowett
M J Watt
John-Olov Jansson
C R Bruce
M A Febbraio
Publicerad i Diabetologia
Volym 53
Nummer/häfte 11
Sidor 2431-2441
ISSN 1432-0428
Publiceringsår 2010
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 2431-2441
Språk en
Länkar dx.doi.org/10.1007/s00125-010-1865-...
Ämnesord Cytokines, Fatty liver, Obesity, Signal transduction, Type 2 diabetes
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

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.

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