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Non alcoholic fatty liver disease (NAFLD) represents a major public health issue as it is currently considered that 20% of the population is at risk in industrialized countries. While NAFLD can remain benign, it predisposes people to more severe pathologies such as steatohepatitis and liver cancer.

Scientists from Toxalim, Research Centre in Food Toxicology (INRA, Toulouse, France), in collaboration with Nanyang Technological University’s Lee Kong Chian School of Medicine (LKCMedicine) in Singapore have provided evidence that the suppression of a protein called PPARα in hepatocytes is sufficient to lead to the development of NAFLD.

These results are published on February 2016 in GUT and Scientific Reports (cf. refrences below).

Context :

• Amongst many key functions, the liver plays a critical part in lipid metabolism. Non alcoholic liver disease or fatty liver relates to abnormally elevated lipid storage in this organ, in the absence of excess alcohol intake. This disease has recently become a major public health issue.

• PPARs (for “Peroxisome Proliferator-Activated Receptors”) are nuclear receptors expressed in many organs (liver, adipose tissues, kidney, muscles…). Stimulated by binding to lipids (fatty acids and their derivatives), a number of drugs and endocrine disruptors (food contaminants), they regulate the expression of a subset of target genes.

• In order to investigate the role of PPARα in liver lipid accumulation, a group of scientists from INRA and LKCMedicine has developed a mouse model lacking the receptor, specifically in the liver.

READ the complete press release in INRA's national website