Hepatocyte-specific deletion of Pparα promotes NAFLD in the context of obesity.
- Régnier, M.
- Polizzi, A.
- Smati, S.
- Lukowicz, C.
- Fougerat, A.
- Lippi, Y.
- Fouché, E.
- Lasserre, F.
- Naylies, C.
- Bétoulières, C.
- Barquissau, V.
- Mouisel, E.
- Bertrand-Michel, J.
- Batut, A.
- Saati, T.A.
- Canlet, C.
- Tremblay-Franco, M.
- Ellero-Simatos, S.
- Langin, D.
- Postic, C.
- Wahli, W.
- Loiseau, N.
- Guillou, H.
- Montagner, A.
DOIAbstract
Peroxisome proliferator activated receptor α (PPARα) acts as a fatty acid sensor to orchestrate the transcription of genes coding for rate-limiting enzymes required for lipid oxidation in hepatocytes. Mice only lacking Pparα in hepatocytes spontaneously develop steatosis without obesity in aging. Steatosis can develop into non alcoholic steatohepatitis (NASH), which may progress to irreversible damage, such as fibrosis and hepatocarcinoma. While NASH appears as a major public health concern worldwide, it remains an unmet medical need. In the current study, we investigated the role of hepatocyte PPARα in a preclinical model of steatosis. For this, we used High Fat Diet (HFD) feeding as a model of obesity in C57BL/6 J male Wild-Type mice (WT)...
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