Journal
CLINICAL SCIENCE
Volume 131, Issue 4, Pages 285-296Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20160469
Keywords
brown adipose tissue; energy expenditure; metabolic syndrome; non-alcoholic fatty liver disease; obesity; thermogenesis
Categories
Funding
- Communaute francaise de Belgique - Actions de Recherche Concertees [12/17-047]
- Fund for Scientific Medical Research [PDRT.1067.14]
- Gilead Belgium
- Janssens Pharmaceutica Belgium
- Roche Belgium
- Belgian National Fund for Scientific Research (FNRS)
- Institut de Recherche experimentale et Clinique (IREC) at the Universite catholique de Louvain, Brussels, Belgium
- Programme d'Excellence Marshall, Wallonia regio
- Universite catholique de Louvain
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Fatty liver diseases are complications of the metabolic syndrome associated with obesity, insulin resistance and low grade inflammation. Our aim was to uncover mechanisms contributing to hepatic complications in this setting. We used foz/foz mice prone to obesity, insulin resistance and progressive fibrosing non-alcoholic steatohepatitis (NASH). Foz/foz mice are hyperphagic but wild-type (WT)-matched calorie intake failed to protect against obesity, adipose inflammation and glucose intolerance. Obese foz/foz mice had similar physical activity level but reduced energy expenditure. Thermogenic adaptation to high-fat diet (HFD) or to cold exposure was severely impaired in foz/foz mice compared with HFD-fed WT littermates due to lower sympathetic tone in their brown adipose tissue (BAT). Intermittent cold exposure (ICE) restored BAT function and thereby improved glucose tolerance, decreased fat mass and liver steatosis. We conclude that failure of BAT adaptation drives the metabolic complications of obesity in foz/foz mice, including development of liver steatosis. Induction of endogenous BAT function had a significant therapeutic impact on obesity, glucose tolerance and liver complications and is a potential new avenue for therapy of non-alcoholic fatty liver disease (NAFLD).
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