Effectiveness of an Innovative Sensory Approach to Improve Children's Nutritional Choices.

A case-control study was conducted to investigate the effectiveness of the Edueat® Method, through experiential workshops focused on the use of all 5 senses. In two different primary schools in the same city, questionnaires were administered in two months with a follow-up one year later. Participants: 119 children (age 8.2-9.0) chosen randomly; control group 66 (55.5%). Seven lessons of 2 h each were held in the schools by experts of the Edueat® method and seven extra lessons by the teachers. The main outcome measures were the children's changes in their approach and attitude towards their eating habits. The answers were grouped with factor analysis and summarized through scores. Repeated-measures analysis of variance was conducted in order to identify the relationships between scores and treatment over time. At the end of treatment, the intervention group showed a significant appreciation towards healthy foods (+4.15 vs. -0.05, p = 0.02) and a greater capacity in identifying foods which are very good for the health (+15.6 vs. +14.4, p = 0.02). In conclusion, the Edueat® method was found to be particularly promising in transmitting knowledge of those foods which are healthy. Greater involvement of teachers and parents is crucial.

GLP-1 Receptor Activation Inhibits Palmitate-Induced Apoptosis via Ceramide in Human Cardiac Progenitor Cells.

Context: Increased apoptosis of cardiomyocytes and cardiac progenitor cells (CPCs) in response to saturated fatty acids (SFAs) can lead to myocardial damage and dysfunction. Ceramides mediate lipotoxicity-induced apoptosis. Glucagonlike peptide-1 receptor (GLP1R) agonists exert beneficial effects on cardiac cells in experimental models. Objective: To investigate the protective effects of GLP1R activation on SFA-mediated apoptotic death of human CPCs. Design: Human CPCs were isolated from cardiac appendages of nondiabetic donors and then exposed to palmitate with or without pretreatment with the GLP1R agonist exendin-4. Ceramide accumulation was evaluated by immunofluorescence. Expression of key enzymes in de novo ceramide biosynthesis was studied by quantitative reverse-transcription polymerase chain reaction and immunoblotting. Apoptosis was evaluated by measuring release of oligonucleosomes, caspase-3 cleavage, caspase activity, and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. Results: Exposure of the CPCs to palmitate resulted in 2.3- and 1.9-fold higher expression of ceramide synthase 5 (CERS5) and ceramide desaturase-1, respectively (P < 0.05). This was associated with intracellular accumulation of ceramide and activation of c-Jun NH2-terminal protein kinase (JNK) signaling and apoptosis (P < 0.05). Both coincubation with fumonisin B1, a specific ceramide synthase inhibitor, and CERS5 knockdown prevented ceramide accumulation, JNK activation, and apoptosis in response to palmitate (P < 0.05). Exendin-4 also prevented the activation of the ceramide biosynthesis and JNK in response to palmitate, inhibiting apoptosis (P < 0.05). Conclusions: Excess palmitate results in activation of ceramide biosynthesis, JNK signaling, and apoptosis in human CPCs. GLP1R activation counteracts this lipotoxic damage via inhibition of ceramide generation, and this may represent a cardioprotective mechanism.