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Endocrine Abstracts (2012) 29 S55.1

Institut Cochin Inserm U1016, Paris, France.


Non-alcoholic fatty liver disease (NAFLD) is gaining increasing recognition as a component of the epidemic of obesity worldwide. The spectrum of NAFLD ranges from simple fatty liver with benign prognosis, to a potentially progressive form, non-alcoholic steatohepatitis (NASH), which may lead to liver fibrosis and cirrhosis, resulting in increased morbidity and mortality. All features of the metabolic syndrome, including obesity, type 2 diabetes, arterial hypertension, and hyperlipidemia are associated with NAFLD/NASH. Despite being potentially severe, little is known about the natural history or prognostic significance of NAFLD. Excessive accumulation of triglycerides in hepatocytes is the hallmark of NAFLD. Despite the existing correlation between fatty liver and insulin resistance it remains unclear whether insulin resistance causes the excessive accumulation of TG in liver or whether the increase in TG or of metabolic intermediates may play a causal role in the development of hepatic or systemic insulin resistance. Studies have reported that the accumulation of intra-hepatic lipids precedes the state of insulin resistance while others showed that hepatic TG themselves are not toxic and may in fact protect the liver from lipotoxicity by buffering the accumulation of deleterious fatty acids. Such findings suggest that hepatic steatosis is not necessarily associated to insulin resistance. In agreement with this concept, some identified population of obese humans can stay free of insulin resistance and are metabolically healthy despite morbid obesity. These findings suggest that not all lipids are detrimental for insulin sensitivity and that specific lipid species, when present in the proper location and time, may trigger signals that modulate adaptation to stress. In the recent years, we have determined the metabolic impact of modulating liver de novo fatty acid synthesis (lipogenesis) via the transcription factor ChREBP on the outcome of hepatic steatosis and/or insulin resistance in mice and humans with NAFLD.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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