The Willingness to Modify Portion Sizes or Eat New Protein Foods Largely Depends on the Dietary Pattern of Protein Intake

International audiencePromoting a more balanced animal/plant dietary protein ratio by changing portion sizes or introducing new foods is a promising means to improve diet quality, but little is known about the willingness of individuals to adopt such changes. Our objective was to assess the willingness to adopt dietary changes by these means. In a French cross-sectional study in 2018 (n = 2055), we analyzed the association between the willingness to eat smaller or larger portions or to introduce non-consumed protein foods and the current dietary patterns of individuals and their socio-demographic characteristics. These modifications had previously been identified as improving the nutrient adequacy of diets. Participants were more willing to eat smaller portion sizes than to introduce new foods and to eat larger portion sizes. The willingness for any modification varied depending on the food groups concerned. Participants were also more willing to eat larger portions and less willing to eat smaller portions when they were the most frequent consumers of the foods concerned. Participants were more willing to eat a new food if it was consumed in large quantities by individuals with a similar dietary pattern. This study underlines the importance of accounting for individual food habits when issuing nutritional recommendations

Unconditional cash transfers do not prevent children's undernutrition in the Moderate Acute Malnutrition Out (MAM'Out) cluster-randomized controlled trial in rural Burkina Faso

International audienceBackground: Limited evidence is available on the impact that unconditional cash transfer (UCT) programs can have on child nutrition, particularly in West Africa, where child undernutrition is still a public health challenge.Objective: This study examined the impact of a multiannual, seasonal UCT program to reduce the occurrence of wasting (weight-for-height, midupper arm circumference), stunting (height-for-age), and morbidity among children 0.05) in children's anthropometric measurements and stunting between the 2 groups at the end point. However, children in the intervention group had a lower risk [21% (95% CI: 18.6%, 21.3%); P < 0.001] of self-reported respiratory tract infections than did children in the control group.Conclusions: We found that seasonal UCTs in the framework of safety nets did not result in a significant decrease in the incidence of acute malnutrition among children in Tapoa Province. Cash transfers combined with complementary interventions targeted to child nutrition and health should be investigated further. This trial was registered at clinicaltrials.gov as NCT01866124

Consequences of PPARα Invalidation on Glutathione Synthesis: Interactions with Dietary Fatty Acids

Glutathione (GSH) derives from cysteine and plays a key role in redox status. GSH synthesis is determined mainly by cysteine availability and γ-glutamate cysteine ligase (γGCL) activity. Because PPARα activation is known to control the metabolism of certain amino acids, GSH synthesis from cysteine and related metabolisms were explored in wild-type (WT) and PPARα-null (KO) mice, fed diets containing either saturated (COCO diet) or 18 : 3 n-3, LIN diet. In mice fed the COCO diet, but not in those fed the LIN diet, PPARα deficiency enhanced hepatic GSH content and γGCL activity, superoxide dismutase 2 mRNA levels, and plasma uric acid concentration, suggesting an oxidative stress. In addition, in WT mice, the LIN diet increased the hepatic GSH pool, without effect on γGCL activity, or change in target gene expression, which rules out a direct effect of PPARα. This suggests that dietary 18 : 3 n-3 may regulate GSH metabolism and thus mitigate the deleterious effects of PPARα deficiency on redox status, without direct PPARα activation

Consequences of PPARα Invalidation on Glutathione Synthesis: Interactions with Dietary Fatty Acids

Glutathione (GSH) derives from cysteine and plays a key role in redox status. GSH synthesis is determined mainly by cysteine availability and γ-glutamate cysteine ligase (γGCL) activity. Because PPARα activation is known to control the metabolism of certain amino acids, GSH synthesis from cysteine and related metabolisms were explored in wild-type (WT) and PPARα-null (KO) mice, fed diets containing either saturated (COCO diet) or 18 : 3 n-3, LIN diet. In mice fed the COCO diet, but not in those fed the LIN diet, PPARα deficiency enhanced hepatic GSH content and γGCL activity, superoxide dismutase 2 mRNA levels, and plasma uric acid concentration, suggesting an oxidative stress. In addition, in WT mice, the LIN diet increased the hepatic GSH pool, without effect on γGCL activity, or change in target gene expression, which rules out a direct effect of PPARα. This suggests that dietary 18 : 3 n-3 may regulate GSH metabolism and thus mitigate the deleterious effects of PPARα deficiency on redox status, without direct PPARα activation

The Nature of the Dietary Protein Impacts the Tissue-to-Diet 15N Discrimination Factors in Laboratory Rats

Due to the existence of isotope effects on some metabolic pathways of amino acid and protein metabolism, animal tissues are 15N-enriched relative to their dietary nitrogen sources and this 15N enrichment varies among different tissues and metabolic pools. The magnitude of the tissue-to-diet discrimination (Δ15N) has also been shown to depend on dietary factors. Since dietary protein sources affect amino acid and protein metabolism, we hypothesized that they would impact this discrimination factor, with selective effects at the tissue level. To test this hypothesis, we investigated in rats the influence of a milk or soy protein-based diet on Δ15N in various nitrogen fractions (urea, protein and non-protein fractions) of blood and tissues, focusing on visceral tissues. Regardless of the diet, the different protein fractions of blood and tissues were generally 15N-enriched relative to their non-protein fraction and to the diet (Δ15N>0), with large variations in the Δ15N between tissue proteins. Δ15N values were markedly lower in tissue proteins of rats fed milk proteins compared to those fed soy proteins, in all sampled tissues except in the intestine, and the amplitude of Δ15N differences between diets differed between tissues. Both between-tissue and between-diet Δ15N differences are probably related to modulations of the relative orientation of dietary and endogenous amino acids in the different metabolic pathways. More specifically, the smaller Δ15N values observed in tissue proteins with milk than soy dietary protein may be due to a slightly more direct channeling of dietary amino acids for tissue protein renewal and to a lower recycling of amino acids through fractionating pathways. In conclusion, the present data indicate that natural Δ15N of tissue are sensitive markers of the specific subtle regional modifications of the protein and amino acid metabolism induced by the protein dietary source

Plant and animal protein intakes are differentially associated with large clusters of nutrient intake that may explain part of their complex relation with cvd risk

International audiencePlant and animal protein intakes are differentially associated with large clusters of nutrient intake that may explain part of their complex relation with cvd ris

Les abondances naturelles des isotopes stables de l'azote chez le rat (facteurs de variabilité et application pour l'étude des flux azotés et de l'impact métabolique de conditions nutritionnelles et physiopathologiques par modélisation compartimentale.)

Les abondances relatives naturelles des différents isotopes stables de l'azote ( 15N) varient selon les tissus au sein d'un individu et selon les individus au sein d'une population, et ces différences reflètent à la fois les caractéristiques de structure et de fonctionnement du métabolisme azoté et ses modulations en lien avec des variations des conditions nutritionnelles et physio-pathologiques. Cette thèse vise, à travers une approche couplée d'expérimentation et de modélisation, à mieux caractériser et comprendre les modulations des 15N des différents pools azotés et à démontrer la capacité des 15N à fournir des informations sur les flux azotés de l'organisme, leurs valeurs et modulations, qui sont encore mal connus. Nous avons, dans un premier temps, mesuré les 15N dans plusieurs tissus (intestin, foie, plasma, muscles, rein, peau...) et dans différentes fractions azotées (acides aminés, protéines, urée, NH4) chez le rat, dans différentes conditions nutritionnelles (chez des rats nourris avec des P de qualité différente, les protéines de lait et de soja) ou physiopathologiques (chez des rats présentant ou non un syndrome métabolique, associant insulino-résistance et obésité, après avoir consommé un même régime potentiellement obésogène). Ces données expérimentales nous ont permis (i) de montrer que l'écart de 15N entre les protéines tissulaires et le régime est plus important lorsque la qualité protéique est moindre, et (ii) de mettre en évidence que, lors de l'initiation précoce d'un syndrome métabolique associant insulino-résistance et obésité, les 15N de certains pools métaboliques sont modulés et constituent des signatures isotopiques des modulations métaboliques associées. Par ailleurs, grâce à l'analyse par modélisation compartimentale des cinétiques de 15N mesurées expérimentalement dans les fractions acides aminés et protéines de différents tissus après augmentation du 15N du régime, nous avons pu estimer les taux de renouvellement protéique tissulaires et explorer la structure et le fonctionnement des échanges entre acides aminés et protéines des différents tissus et comparer leur degré de compartimentation. Enfin, nous avons développé un modèle multi-compartimental reproduisant l'ensemble des flux azotés inter- et intra-organes de l'organisme et rendant compte des variations de 15N observées. Cette représentation globale du métabolisme azoté fournit une vision novatrice du fonctionnement intégré du métabolisme azoté dont les données éparses de la littérature ne donnaient auparavant qu'une vision parcellaire et fragmentée. Le modèle a permis de reconstituer les mécanismes qui conduisent à l'observation de différences de 15N entre pools azotés, de mieux comprendre quelles modulations sont les plus susceptibles d'affecter les 15N, avec quelle amplitude et dans quel sens, et finalement d'expliquer les variations de 15N mises en évidence expérimentalement en terme de modulation des flux azotés. L'ensemble de nos résultats d'expérimentation et de modélisation démontre la capacité des 15N à apporter des informations sur les flux métaboliques azotés et souligne l'intérêt prometteur de cette approche nouvelle pour acquérir une compréhension intégrée du système complexe du métabolisme azoté inter- et intra-organes et des processus homéostatiques qui le régulent et de ses dérégulations pré-pathologiques.Natural abundances of stable nitrogen isotopes vary among tissues within an individual and among individuals within a population, and these differences are linked to the structural and functioning characteristics of the nitrogen metabolism and also to its modulations in response to variations in nutritional and physiological conditions. In this thesis, we developed an approach combining both experimentation and modeling, in order to better characterize and understand the modulations in the 15N values of various nitrogen metabolic pools, and to show the capacity of the 15N to provide information regarding the values and modulations of the body nitrogen fluxes, that are still poorly determined. We first measured the 15N in various tissues (intestine, liver, plasma, muscle, kidney, skin ) and in various nitrogen fractions (amino acids, proteins, urea, NH4) in rats, under different nutritional (i.e. in rats fed with P of distinct quality, that were milk and soy P) or pathophysiological (i.e. in rats that had or not become obese and insulin resistant after being fed a high-fat diet for 10 weeks). From these experimental data, we showed (i) that the tissue nitrogen discrimination (i.e., the difference between tissue and diet 15N) is higher when the P is of lesser quality, and (ii) that, during the onset of a metabolic syndrome, in the presence of both insulin resistance and obesity, the 15N differed in some nitrogen pools and thus constitute isotopic signatures of the metabolic impact of such conditions. In this thesis, we also measured the 15N kinetics in the amino acid and protein fractions of several tissues after a shift in the diet 15N. The analysis of these kinetics, using a compartimental modeling approach, enabled us to estimate tissue fractional turnover rates and to investigate the structure and the functioning of the protein synthesis and breakdown exchanges in some tissues and their level of compartmentation. Lastly, we developed a multi-compartmental model that describes the various body nitrogen transfers between and within tissues and accounts for the observed 15N variability. This model of the nitrogen metabolism provides a new and systemic insight of the interactions and modulations of the various nitrogen fluxes, as opposed to the fragmented information available from the literature data. This model enabled us to reconstruct the mechanisms that caused the observed 15N differences between nitrogen pools, to better understand how they vary, depending on which metabolic modulation and with which amplitude, and finally to hypothesize which nitrogen fluxes alterations are the more likely to be responsible for the 15N variations that we observed in our experimentations. In conclusion, our experimental and modelling results show that it is feasible to gain information from the 15N values regarding the metabolic nitrogen fluxes and their modulations, and highlight the interest of this new approach to get an integrated insight into the complex nitrogen metabolic system and a better understanding of the way the various between and within tissues nitrogen fluxes are regulated and altered.PARIS-AgroParisTech Centre Paris (751052302) / SudocSudocFranceF

Invited commentary in response to: Risk of overestimating treatment effects and generalisability of computer-based tailored dietary counselling

International audienceWe appreciate the comments received from Okami et al. (1) on our recently-published article, which reports the results of a study to determine whether, and to what extent, a guided, stepwise and tailored dietary counselling programme could better improve the nutrient adequacy of the diet compared to an approach based solely on generic guidelines (2). Our study was conducted in pregnant, French women

Caractérisation d un modèle de dysfonction endothéliale postprandiale chez le rat sain (intérêt de la modulation de la nature des protéines en termes de prévention du risque cardiovasculaire)

PARIS-AgroParisTech Centre Paris (751052302) / SudocSudocFranceF