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Dietary fibers (DF) are important components of human and animal diets. However, they can decrease protein digestibility and absorption and thus the nutritional value of a food. The aim of this study was to investigate how the form of delivery of pea DF impacted the integrity of the intestinal barrier and, thereby, the potential absorption of molecules. To this end, two pea flours, with either intact or ruptured cell walls, and two controls, pea fibers and pea protein, were digested in vitroand the digesta obtained applied onto a jejunum porcine cell line (IPEC-J2 cells). Cell viability and integrity were evaluated by transepithelial electrical resistance measurement, colorimetric assay (MTS), and immunohistochemistry for tight junction proteins. Additionally, the diffusion of FITC-dextran (FD4) and lucifer yellow (LY) through the epithelial cell monolayers was monitored. The digested pea samples did not alter the IPEC-J2 viability and permeability. For instance, no difference in the diffusion of molecules either FD4 or LY across the monolayers was observed between the different digesta and the control. Similarly, no effect was observed in ZO-1 labeling intensity compared to the control. This study demonstrated that intestinal integrity was maintained whether pea cell walls were intact or ruptured.

Background: Early hyperphagia and hypothalamic inflammation encountered after Western diet (WD) are linked to rodent propensity to obesity. Inflammation in several brain structures has been associated with gut dysbiosis. Since gut microbiota is highly sensitive to dietary changes, we hypothesised that immediate gut microbiota adaptation to WD in rats is involved in inflammation-related hypothalamic modifications. Methods: We evaluated short-term impact of WD consumption (2 h, 1, 2 and 4 days) on hypothalamic metabolome and caecal microbiota composition and metabolome. Data integration analyses were performed to uncover potential relationships among these three datasets. Finally, changes in hypothalamic gene expression in absence of gut microbiota were evaluated in germ-free rats fed WD for 2 days. Results: WD quickly and profoundly affected the levels of several hypothalamic metabolites, especially oxidative stress markers. In parallel, WD consumption reduced caecal microbiota diversity, modified its composition towards pro-inflammatory profile and changed caecal metabolome. Data integration identified strong correlations between gut microbiota sub-networks, unidentified caecal metabolites and hypothalamic oxidative stress metabolites. Germ-free rats displayed reduced energy intake and no changes in redox homoeostasis machinery expression or pro-inflammatory cytokines after 2 days of WD, in contrast to conventional rats, which exhibited increased SOD2, GLRX and IL-6 mRNA levels. Conclusion: A potentially pro-inflammatory gut microbiota and an early hypothalamic oxidative stress appear shortly after WD introduction. Tripartite data integration highlighted putative links between gut microbiota sub-networks and hypothalamic oxidative stress. Together with the absence of hypothalamic modifications in germ-free rats, this strongly suggests the involvement of the microbiota-hypothalamus axis in rat adaptation to WD introduction and in energy homoeostasis regulation.

Le glucagon-like peptide 1 (GLP-1) et le peptide tyrosine-tyrosine (PYY) sont deux hormones intestinales impliquées dans le métabolisme. Elles sont secrétées en présence d’acides gras à chaîne courte (AGCC) produits par le microbiote intestinal et sont des acteurs majeurs de l’axe microbiote-intestin-cerveau. Malgré l’intérêt croissant porté à la programmation nutritionnelle, la façon dont cet axe et la fonction endocrine intestinale se mettent en place chez le nouveau-né reste mal connue, notamment dans des contextes nutritionnels différents. Le but de notre étude était donc d’étudier cette mise en place chez le miniporc Yucatan comme modèle du nouveau-né humain. Trente-six porcelets allaités par leur mère (A) ont été euthanasiés à 0, 2, 5 et 10jours d’âge. 21 autres porcelets ont été nourris dès la naissance avec une préparation pour nourrisson (PPN) contenant soit des lipides laitiers (LL), soit des lipides végétaux (LV), et euthanasiés à J10. La maturation de la fonction endocrine intestinale s’est caractérisée par une diminution de l’expression du gène codant pour la convertase 1/3 (PCSK1), enzyme permettant de cliver le proglucagon en GLP-1 actif, ainsi que de l’expression des gènes du PYY et de la chromogranine A (CHGA), un marqueur générique des cellules endocrines. Cette diminution apparaissait dès J2 dans l’iléon, plus tardivement dans le côlon. La quantité de GLP-1 contenue dans l’iléon et le côlon diminuait dès J2 tandis que la concentration plasmatique de GLP-1 diminuait à partir de J5. Les PPN n’ont pas modifié l’expression de PCSK1, PYY ou CHGA à J10, mais ont augmenté l’expression du gène FFAR2 qui code un récepteur aux AGCC par rapport aux porcelets A, de même que le contenu en GLP-1 de l’iléon, du côlon, et du plasma. De plus, l’expression des récepteurs au GLP-1 et au PYY était diminuée dans l’hypothalamus des porcelets LL et LV par rapport aux porcelets A. La fonction endocrine intestinale évolue très rapidement chez le nouveau-né et de façon séquentielle le long du tube digestif. En effet, des PPN contenant soit des LL soit des LV ont eu un impact majeur sur ce développement, au niveau intestinal mais aussi cérébral. Cela confirme que les premiers jours de vie constituent une fenêtre critique pour la programmation de la santé.

Our study aimed at investigating the impact of the level of protein in milk formula on intestinal structure, barrier function, and its nervous regulation in normal and LBW neonates using a porcine model. Normal birth weight (NBW) or LBW piglets were fed from d7 to d28 of age either with a high protein (HP) or with an adequate protein (AP) formula or stayed with their mother mother fed (MF). The proximal jejunum and distal ileum were sampled at d28 for morphometry analysis and ex vivopermeability measurement in Ussing chambers. Formula feeding induced a trophic effect on the jejunum and ileum of both NBW and LBW piglets, which exhibited longer villi than MF animals, irrespective of the type of formula. In NBW piglets, intestinal permeability was not altered by formula feeding. On the contrary, LBW piglets fed with HP formula, but not AP, exhibited a greater ileal permeability than MF piglets. Feeding the HP formula also disturbed jejunal and ileal regulation of permeability by acetylcholine and vasoactive intestinal peptide (VIP) in LBW compared with MF LBW piglets. In conclusion, the level of protein in formulas did not modify intestinal structure and function in NBW individuals but dramatically modified intestinal barrier function physiology in LBW individuals.

Our study aimed at investigating the impact of the level of protein in milk formula on intestinal structure, barrier function, and its nervous regulation in normal and LBW neonates using a porcine model. Normal birth weight (NBW) or LBW piglets were fed from d7 to d28 of age either with a high protein (HP) or with an adequate protein (AP) formula or stayed with their mother [mother fed (MF)]. The proximal jejunum and distal ileum were sampled at d28 for morphometry analysis and ex vivo permeability measurement in Ussing chambers. Formula feeding induced a trophic effect on the jejunum and ileum of both NBW and LBW piglets, which exhibited longer villi than MF animals, irrespective of the type of formula. In NBW piglets, intestinal permeability was not altered by formula feeding. On the contrary, LBW piglets fed with HP formula, but not AP, exhibited a greater ileal permeability than MF piglets. Feeding the HP formula also disturbed jejunal and ileal regulation of permeability by acetylcholine and vasoactive intestinal peptide (VIP) in LBW compared with MF LBW piglets. In conclusion, the level of protein in formulas did not modify intestinal structure and function in NBW individuals but dramatically modified intestinal barrier function physiology in LBW individuals.

To support rapid growth and a high metabolic rate, infants require enormous amounts of nutrients. The small intestine must have the complete array of transporters that absorb the nutrients released from digested food. Failure of intestinal transporters to function properly often presents symptoms as “failure to thrive” because nutrients are not absorbed and as diarrhea because unabsorbed nutrients upset luminal osmolality or become substrates of intestinal bacteria. We enumerate the nutrients that constitute human milk and various infant milk formulas, explain their importance in neonatal nutrition, then describe for each nutrient the transporter(s) that absorbs it from the intestinal lumen into the enterocyte cytosol and from the cytosol to the portal blood. More than 100 membrane and cytosolic transporters are now thought to facilitate absorption of minerals and vitamins as well as products of digestion of the macronutrients carbohydrates, proteins, and lipids. We highlight research areas that should yield information needed to better understand the important role of these transporters during normal development.

To support rapid growth and a high metabolic rate, infants require enormous amounts of nutrients. The small intestine must have the complete array of transporters that absorb the nutrients released from digested food. Failure of intestinal transporters to function properly often presents symptoms as “failure to thrive” because nutrients are not absorbed and as diarrhea because unabsorbed nutrients upset luminal osmolality or become substrates of intestinal bacteria. We enumerate the nutrients that constitute human milk and various infant milk formulas, explain their importance in neonatal nutrition, then describe for each nutrient the transporter(s) that absorbs it from the intestinal lumen into the enterocyte cytosol and from the cytosol to the portal blood. More than 100 membrane and cytosolic transporters are now thought to facilitate absorption of minerals and vitamins as well as products of digestion of the macronutrients carbohydrates, proteins, and lipids. We highlight research areas that should yield information needed to better understand the important role of these transporters during normal development.

Incidence of diarrhea at weaning in commercial pigs is an important problem, and diet is thought to be a predisposing factor. The aim of this study was to determine the impact of switching from milk-based to cereal-based diets on the morphology and function of the small intestine of piglets using a model of delayed weaning to isolate the influence of the diet from that of environmental and social factors.

Incidence of diarrhea at weaning in commercial pigs is an important problem, and diet is thought to be a predisposing factor. The aim of this study was to determine the impact of switching from milk-based to cereal-based diets on the morphology and function of the small intestine of piglets using a model of delayed weaning to isolate the influence of the diet from that of environmental and social factors. Forty-five piglets received a milk-based diet for 5 weeks after weaning. Thirty piglets were then switched from milk-based to wheat- or barley-based diets, mimicking the dietary change that occurs at weaning. The last 15 piglets remained on the milk-based diet. Piglets were killed 4 days after the dietary switch. Jejunal mucosa morphometry and enzyme activities were measured. Ussing chambers were used to measure intestinal permeability to macromolecules, basal electrical properties, glucose absorption, and induced chloride-secretion. Alkaline phosphatase– and sucrase-specific activities were higher in both groups of cereal-fed piglets than in milk-fed piglets. Dipeptidylpeptidase IV activity was higher in wheat-fed piglets than in the other groups. Na+-dependent glucose absorption was 1.7-fold higher in cereals-fed piglets than in milk-fed piglets. Serotonin-induced and vasoactive intestinal polypeptide–induced chloride secretion was doubled in cereals-fed piglets. Dietary transition did not influence the other parameters. These results indicate that switching from milk to cereals increased some mucosal enzyme activities, intestinal Na+–dependent glucose absorption, and response to secretagogues. This supports the hypothesis that dietary factors could initiate diarrhea in the presence of other aggravating factors, such as pathogens or environmental stress.