Adherence to Mediterranean diet is inversely associated with the consumption of ultra-processed foods among Spanish children: the SENDO project.

OBJECTIVE: To assess whether higher adherence to the traditional Mediterranean diet (MedDiet) was associated with lower consumption of ultra-processed foods (UPF) and lower free sugar intake. DESIGN: Cross-sectional analysis of baseline information among participants in the SENDO project, a Spanish paediatric cohort. Dietary information was collected through a semi-quantitative FFQ. Food items were classified according to the NOVA classification. Adherence to the MedDiet was evaluated through the KIDMED index. SETTING: Spain. PARTICIPANTS: Three hundred eight-six children (52 % boys) with a mean age of 5·3 years old (sd 1·0) were included in the analysis. RESULTS: 74·4 % of the children had moderate adherence to the MedDiet (mean KIDMED score: 5·9 points; sd 1·7) and overall, 32·2 % of the total energy intake came from UPF. Each two additional points in the KIDMED score was associated with 3·1 % (95 % CI 2·1, 4·0) lower energy intake from UPF. Compared to those with low adherence to the MedDiet, children with medium and high adherence reported 5·0 % (95 % CI 2·2, 7·7) and 8·5 % (95 % CI 5·2, 11·9) lower energy intake from UPF, respectively. We also found that 71·6 % of the variability in free sugar intake was explained by the variability in UPF consumption. CONCLUSIONS: Adherence to the traditional MedDiet was inversely associated with energy intake from UPF. Furthermore, most of the variability in free sugar intake was explained by the variability of UPF consumption. Public health strategies are needed to strengthen the adherence to the MedDiet in pre-schoolers while regulating the production, marketing and advertising of UPF.

The cellular prion protein PrPc is a partner of the Wnt pathway in intestinal epithelial cells.

We reported previously that the cellular prion protein (PrP(c)) is a component of desmosomes and contributes to the intestinal barrier function. We demonstrated also the presence of PrP(c) in the nucleus of proliferating intestinal epithelial cells. Here we sought to decipher the function of this nuclear pool. In human intestinal cancer cells Caco-2/TC7 and SW480 and normal crypt-like HIEC-6 cells, PrP(c) interacts, in cytoplasm and nucleus, with γ-catenin, one of its desmosomal partners, and with ß-catenin and TCF7L2, effectors of the canonical Wnt pathway. PrP(c) up-regulates the transcriptional activity of the ß-catenin/TCF7L2 complex, whereas γ-catenin down-regulates it. Silencing of PrP(c) results in the modulation of several Wnt target gene expressions in human cells, with different effects depending on their Wnt signaling status, and in mouse intestinal crypt cells in vivo. PrP(c) also interacts with the Hippo pathway effector YAP, suggesting that it may contribute to the regulation of gene transcription beyond the ß-catenin/TCF7L2 complex. Finally, we demonstrate that PrP(c) is required for proper formation of intestinal organoids, indicating that it contributes to proliferation and survival of intestinal progenitors. In conclusion, PrP(c) must be considered as a new modulator of the Wnt signaling pathway in proliferating intestinal epithelial cells.