Overweight and obesity are considered as risk factors for hepatocellular carcinoma(HCC) development. The mechanisms by which obesity promotes liver inflammationare however poorly understood. We recently generated a full DUSP3 knockout (KO)mouse. The obtained mice were born normal with no spontaneous phenotype.However, while aging, DUSP3-KO mice became obese and developedhepatosteatosis. The phenotype was exacerbated under high fat diet (HFD).Furthermore, when treated with diethylnitrosamine (DEN) procarcinogen, DUSP3-KOmice developed HCC faster than WT littermates. The combination of DEN with HFDaccelerated the onset of HCC development in these mice compared to WT mice. Thiswas associated with increased systemic levels of several metabolites and withhyperphosphorylation of the insulin-like growth factor receptor I.
نوع الوثيقة:
conferencePoster
اللغة:
English
Relation:
Sophie Jacques, Paris, France (23 juillet 2017 au 28 juillet 2017)
