Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
o abstract
ISSN: 0168-8278

hal-01519257
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01519257
DOI : 10.1016/S0168-8278(16)00178-1

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
Cell death of hepatocytes is a prominent characteristic in the pathogenesis of liver disease, while hepatolysis is a starting point of inflammation in hepatitis and loss of hepatic function. However, the precise molecular mechanisms of hepatocyte cell death, the role of the cytokines of hepatic microenvironment and the involvement of intracellular kinases, remain unclear. Tumor necrosis factor alpha (TNF-α) is a key cytokine involved in cell death or survival pathways and the role of RIPK1 has been associated to the TNF-α-dependent signaling pathway. We took advantage of two different deficient mouse lines, the RIPK1 kinase dead knock-in mice (Ripk1K45A) and the conditional knockout mice lacking RIPK1 only in liver parenchymal cells (Ripk1LPC-KO), to characterize the role of RIPK1 and TNF-α in hepatitis induced by concanavalin A (ConA). Our results show that RIPK1 is dispensable for liver homeostasis under steady-state conditions but in contrast, RIPK1 kinase activity contributes to caspase-independent cell death induction following ConA injection and RIPK1 also serves as a scaffold, protecting hepatocytes from massive apoptotic cell death in this model. In the Ripk1LPC-KO mice challenged with ConA, TNF-α triggers apoptosis, responsible for the observed severe hepatitis. Mechanism potentially involves both TNF-independent canonical NF-κB activation, as well as TNF-dependent, but canonical NF-κB-independent mechanisms. In conclusion, our results suggest that RIPK1 kinase activity is a pertinent therapeutic target to protect liver against excessive cell death in liver diseases. © The Author(s) 2016.
ISSN: 2041-4889

hal-01414916
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01414916
DOI : 10.1038/cddis.2016.362
PUBMED : 27831558

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
Background Although the French eating model may differ from those of other countries, no studies to date have investigated dietary patterns in a wide age range of adults and at the national level. We aimed to identify dietary patterns (DP) of French adults and assess their associations with demographic, socio-economic and behavioural factors. Methods The present study included 2624 adults (1087 men, 1537 women) aged 18–79 years from the cross-sectional national French INCA2 dietary survey. Dietary data were collected using a 7-day estimated food record. Clusters of DP were derived using principal component analysis and clustering, conjointly. Age-adjusted logistic regression analyses were used to investigate the association between DP and correlates. Results Five DP were identified, namely ‘traditional’, ‘prudent’, ‘diversified’, ‘processed’ and ‘sandwiches’. Men were more likely to follow a traditional diet and women the ‘prudent’ pattern. Members of the ‘processed’ and ‘sandwiches’ patterns were younger compared to non-members. Healthier dietary patterns were overall positively associated with a higher socio-economic position, healthier behaviours (in terms of sedentary behaviours and smoking status) and lower body mass index. Under-reporting of energy intake, restrictive diet to lose weight and dietary supplement consumption were also related to specific DP, although differentially in men and women. Associations with contextual factors (i.e. household composition, agglomeration size and region) were also observed. Conclusions The identification of adults’ dietary patterns and associated behaviours (all modifiable) is important for the conceptualisation of multi-behavioural programs. The additional information on social and environmental correlates is also essential for targeting the most vulnerable population groups in the context of such public health interventions
ISSN: 0952-3871

hal-01299975
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01299975
DOI : 10.1111/jhn.12315
PUBMED : 25233099