Journal of Liver

p38γ and p38δ reprogram liver metabolism by modulating neutrophil infiltration

2^nd International Conference on Hepatology

May 09-11, 2016 Chicago, USA

Guadalupe Sabio

National Center for Cardiovascular Research, Spain

Posters & Accepted Abstracts: J Liver

Abstract:

Nonalcoholic fatty liver disease (NAFLD) is a major health problem and the main cause of liver disease in Western countries. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood. The disease begins with an excessive accumulation of triglycerides in the liver, which stimulates an inflammatory response. Alternative p38 mitogen-activated kinases (p38�?�?�?³ and p38�?�?�?´), have been shown to contribute to inflammation in different diseases. Here we demonstrate that p38�?�?�?´ is elevated in livers of obese patients with NAFLD and that mice lacking p38�?�?�?³/�?�?�?´ in myeloid cells are resistant to diet-induced fatty liver, hepatic triglyceride accumulation and glucose intolerance. This protective effect is due to defective migration of p38�?�?�?³/�?�?�?´-deficient neutrophils to the damaged liver. We further show that neutrophil infiltration in wild-type mice contributes to steatosis development by means of inflammation and liver metabolic changes. Therefore, p38�?�?�?³ and p38�?�?�?´ in myeloid cells provide a potential target for NAFLD therapy.

Biography :

Email: guadalupe.sabio@cnic.es