Journal
PLOS ONE
Volume 11, Issue 6, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0157956
Keywords
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Categories
Funding
- Instituto de Salud Carlos III, Red de Trastornos Adictivos UE-FEDER [RD12/0028/0001]
- Ministerio de Economia y Competitividad [PI13/02261]
- Ministerio de Sanidad, Servicios Sociales e Igualdad, Plan Nacional sobre Drogas [049/2009, 049/2013]
- Consejeria de Economia, Innovacion y Ciencia, Junta de Andalucia [CTS-433]
- Consejeria de Salud y Bienestar Social, Junta Andalucia [PI0552, PI0228-2013, PI0823-2012]
- National System of Health, Instituto de Salud Carlos III [CP12/03109, CP14/00212, CP14/00173]
- Program of the Instituto de Salud Carlos III
- Andalusian Progreso y Salud Foundation, Spain
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High-fat diet-induced obesity (DIO) is associated with fatty liver and elevated IL-6 circulating levels. IL-6 administration in rodents has yielded contradictory results regarding its effects on steatosis progression. In some models of fatty liver disease, high doses of human IL-6 ameliorate the liver steatosis, whereas restoration of IL-6 in DIO IL-6(-/-) mice up-regulates hepatic lipogenic enzymes and aggravates steatosis. We further examined the effects of chronic low doses of murine IL-6 on hepatic lipid metabolism in WT mice in DIO. IL-6 was delivered twice daily in C57BL/6J DIO mice for 15 days. The status and expression of IL-6 signalling mediators and targets were investigated in relation to the steatosis and lipid content in blood and in liver. IL-6 administration in DIO mice markedly raised circulating levels of lipids, glucose and leptin, elevated fat liver content and aggravated steatosis. Under IL-6 treatment there was hepatic Stat3 activation and increased gene expression of Socs3 and Tnf-alpha whereas the gene expression of endogenous IL-6, IL-6-receptor, Stat3, Cpt1 and the enzymes involved in lipogenesis was suppressed. These data further implicate IL-6 in fatty liver disease modulation in the context of DIO, and indicate that continuous stimulation with IL-6 attenuates the IL-6-receptor response, which is associated with high serum levels of leptin, glucose and lipids, the lowering levels of lipogenic and Cpt1 hepatic enzymes and with increased Tnf-alpha hepatic expression, a scenario evoking that observed in IL-6(-/-) mice exposed to DIO and in obese Zucker rats.
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