European public health best practice portal - process and criteria for best practice assessment.

BACKGROUND: Non-communicable diseases (NCDs) are major and growing burden on population health and the use and cost of healthcare in EU Member States and beyond. Different countries face many common challenges in public health and can learn from each other. The exchange of 'best practices' is one way to tackle the observed disparities in health sector. To address the United Nations Sustainable Development Goals, the European Commission developed the EU Public Health Best Practice Portal to facilitate the exchange of best practices and facilitate their implementation in other EU countries or regions. The ultimate aim of the portal is to reduce NCDs burden and the prevalence of their risk factors by promoting implementation and scale up of evidence-based effective interventions in the areas of health promotion, disease prevention and management of NCDs. RESULTS: This article presents the rationale and the process, ranging from best practice assessment to their transfer to interested Member States, applied in the EU Public Health Best Practice Portal. The portal selects best practices using rigorously defined criteria for best practice assessment. This article further provides an overview of other similar initiatives in Europe and internationally that collect and disseminate information on interventions and actions to combat NCDs. CONCLUSION: Exchange of best practices is a promising tool in tackling NCDs. Transfer and scaling up of policies and interventions between countries may contribute to tackle disparities observed between countries in regards to the prevalence of risk factors and associated diseases.

Increasing protein at the expense of carbohydrate in the diet down-regulates glucose utilization as glucose sparing effect in rats.

High protein (HP) diet could serve as a good strategy against obesity, provoking the changes in energy metabolic pathways. However, those modifications differ during a dietary adaptation. To better understand the mechanisms involved in effect of high protein diet (HP) on limiting adiposity in rats we studied in parallel the gene expression of enzymes involved in protein and energy metabolism and the profiles of nutrients oxidation. Eighty male Wistar rats were fed a normal protein diet (NP, 14% of protein) for one week, then either maintained on NP diet or assigned to a HP diet (50% of protein) for 1, 3, 6 and 14 days. mRNA levels of genes involved in carbohydrate and lipid metabolism were measured in liver, adipose tissues, kidney and muscles by real time PCR. Energy expenditure (EE) and substrate oxidation were measured by indirect calorimetry. Liver glycogen and plasma glucose and hormones were assayed. In liver, HP feeding 1) decreased mRNA encoding glycolysis enzymes (GK, L-PK) and lipogenesis enzymes(ACC, FAS), 2) increased mRNA encoding gluconeogenesis enzymes (PEPCK), 3) first lowered, then restored mRNA encoding glycogen synthesis enzyme (GS), 4) did not change mRNA encoding ß-oxidation enzymes (CPT1, ACOX1, ßHAD). Few changes were seen in other organs. In parallel, indirect calorimetry confirmed that following HP feeding, glucose oxidation was reduced and fat oxidation was stable, except during the 1(st) day of adaptation where lipid oxidation was increased. Finally, this study showed that plasma insulin was lowered and hepatic glucose uptake was decreased. Taken together, these results demonstrate that following HP feeding, CHO utilization was increased above the increase in carbohydrate intake while lipogenesis was decreased thus giving a potential explanation for the fat lowering effect of HP diets.

Postprandial nutrient partitioning but not energy expenditure is modified in growing rats during adaptation to a high-protein diet.

It has been suggested that high-protein (HP) diets may favor weight management by lowering energy intake and reducing body fat. Whether these effects result from changes in energy metabolism remains unclear. We measured the adaptation of energy metabolism components during 2 wk of HP feeding. Fifty male Wistar rats were switched from a control diet to an HP diet (14 and 55% of protein, respectively) for 1, 3, 6, or 14 d. Energy expenditure (EE) and substrate oxidation were measured by indirect calorimetry in feed-deprived rats and after consumption of a test meal. EE components, including the thermic effect of feeding and activity, were not modified during adaptation to an HP diet. Nutrient oxidation in feed-deprived rats was not affected by HP feeding, except for an early increase in protein oxidation. After 1 d, the postprandial inhibition of lipid oxidation (Lox) was blunted, carbohydrate (CHO) oxidation decreased by one-half, and urea clearance decreased by 66%. Thereafter, CHO oxidation gradually rose, resulting in a null CHO balance. Lox and urea clearance recovered after 3 d of adaptation to an HP diet, while protein oxidation reached a plateau. The postprandial oxidation of CHO counterbalanced the amount of ingested CHO as soon as 3 d, leading to a null postprandial CHO balance. We conclude that the inhibition of de novo lipogenesis from dietary CHO, but not EE and Lox, may participate in limiting the adiposity induced by HP feeding. The transient changes occurring during the period of adaptation to the diet highlight that the duration of the diet is critical in HP diet studies.