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Reducing the CP content and increasing the fermentable carbohydrates (FC) content of the diet may counteract the negative effects of protein fermentation in newly weaned piglets fed high-CP diets. To study the synergistic effects of CP and FC on gut health and its consequences for growth performance, 272 newly weaned piglets (26 d of age, 8.7 kg of BW) were allotted to 1 of 4 dietary treatments in a 2 x 2 factorial arrangement, with low and high CP and low and high FC content as the factors. Eight piglets from each dietary treatment were killed on d 7 postweaning. Feces and digesta from ileum and colon were collected to determine nutrient digestibility, fermentation products, and microbial counts. In addition, jejunum tissues samples were collected for intestinal morphology and enzyme activity determination. During the entire 4-wk period, interactions between the dietary CP and FC contents were found for ADFI (P = 0.022), ADG (P = 0.001), and G:F (P = 0.033). The high-FC content reduced ADFI, ADG, and G:F in the low-CP diet, whereas the FC content did not affect growth performance in the high-CP diet. Lowering the CP content of the low-FC diet improved ADFI and ADG, whereas lowering the CP content of the high-FC diet did not influence growth performance. The low-CP diets resulted in a lower concentration of ammonia in the small intestine (P = 0.003), indicating reduced protein fermentation. In the small intestine, the high FC content increased the number of lactobacilli (P = 0.047), tended to decrease the number of coliforms (P = 0.063), tended to increase the lactic acid content (P = 0.080), and reduced the concentration of ammonia (P = 0.049). In the colon, the high-FC diets increased the concentration of total VFA (P = 0.009), acetic acid (P = 0.003), and butyric acid (P = 0.018), and tended to decrease the ammonia concentration (P = 0.076). Intestinal morphology and activity of brush border enzymes were not affected by the diet, although maltase activity tended to decrease with increasing dietary FC (P = 0.061). We concluded that an increase in the dietary FC content, and to a lesser extent a decrease in the CP content, reduced ammonia concentrations and altered the microflora and fermentation patterns in the gastrointestinal tract of weaned piglets. However, these effects were not necessarily reflected by an increased growth performance of the piglets. Key words: fermentable carbohydrate, growth, intestinal health, piglet, protein, weaning

Transition from sow's milk to solid feed is associated with intestinal atrophy and diarrhea. We hypothesized that the intestinotrophic hormone glucagon-like peptide 2 (GLP-2) would induce a dose- and health status-dependent effect on gut adaptation. In Exp. 1, weaned pigs (average BW at weaning 4.98 ±0.18 kg) were kept in a high-sanitary environment and injected with saline or short-acting GLP-2 (80 ug/(kg BW-12 h); n = 8). Under these conditions, there was no diarrhea and GLP-2 did not improve gastrointestinal structure or function. In Exp. 2, weaned pigs (average BW at weaning 6.68 ± 0.27 kg) were kept in a low-sanitary environment, leading to weaning diarrhea, and injected with saline or short-acting GLP-2 (200 ug/(kg BW-12 h); n = 11). Treatment with GLP-2 increased goblet cell density (P < 0.05) and reduced short chain fatty acid concentration in the colon (P < 0.01) but had limited effects on diarrhea. In Exp. 3, weaned pigs (average BW at weaning 6.90 ± 0.32 kg) were kept in a low-sanitary environment and injected with saline or a long-acting acylated GLP-2 analogue (25 ug/(kg BW-12 h); n = 8). In this experiment, GLP-2 increased intestinal weight (+22%; P < 0.01) and activity of brush border enzymes (+50-100%; P < 0.05). Circulating GLP-2 levels were in the pharmacological range in Exp. 3 (constant levels >20,000 pmol/L) and Exp. 2 (increases to 20,000 pmol/L for a few hours each day) while they were in the supraphysi-ological range in Exp. 1 (50-200 pmol/L). In conclusion, GLP-2 may improve gut structure and function in weanling pigs. However, the effects may be significant only under conditions of diarrhea and if GLP-2 exposure time is extended using long-acting analogues. [ABSTRACT FROM AUTHOR]

A specific method for pancreatic elastase II activity analysis was developed. True elastase II activity could be discriminated from that of elastase I and chymotrypsin. The postnatal development of four pancreatic proteases in the duodenal juice of children and in the pancreatic homogenates of calves and piglets was measured. The study was carried out on patients without (14 children) and with (5 children) pancreatic insufficiency. Calves and piglets were either milk-fed or weaned until slaughter at different ages. Profiles of enzyme development were globally similar in milk-fed piglets and calves, while in children without pancreatic insufficiency, no significant change was observed between 4 and 168 months. In children with pancreatic insufficiency, enzyme activity was low. In animals, elastase II and chymotrypsin activities were maximal at birth, decreased with age, and probably were associated with the digestion of milk protein. In contrast, elastase I and trypsin activities increased markedly after weaning in connection with the intake of solid food. [ABSTRACT FROM AUTHOR]

The assembly of the newborn's gut microbiota during the first months of life is an orchestrated process resulting in specialized microbial ecosystems in the different gut compartments. This process is highly dependent upon environmental factors, and many evidences suggest that early bacterial gut colonization has long-term consequences on host digestive and immune homeostasis but also metabolism and behavior. The early life period is therefore a "window of opportunity" to program health through microbiota modulation. However, the implementation of this promising strategy requires an in-depth understanding of the mechanisms governing gut microbiota assembly. Breastfeeding has been associated with a healthy microbiota in infants. Human milk is a complex food matrix, with numerous components that potentially influence the infant microbiota composition, either by enhancing specific bacteria growth or by limiting the growth of others. The objective of this review is to describe human milk composition and to discuss the established or purported roles of human milk components upon gut microbiota establishment. Finally, the impact of maternal diet on human milk composition is reviewed to assess how maternal diet could be a simple and efficient approach to shape the infant gut microbiota., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Boudry, Charton, Le Huerou-Luron, Ferret-Bernard, Le Gall, Even and Blat.)

The present review examines the pig as a model for physiological studies in human subjects related to nutrient sensing, appetite regulation, gut barrier function, intestinal microbiota and nutritional neuroscience. The nutrient-sensing mechanisms regarding acids (sour), carbohydrates (sweet), glutamic acid (umami) and fatty acids are conserved between humans and pigs. In contrast, pigs show limited perception of high-intensity sweeteners and NaCl and sense a wider array of amino acids than humans. Differences on bitter taste may reflect the adaptation to ecosystems. In relation to appetite regulation, plasma concentrations of cholecystokinin and glucagon-like peptide-1 are similar in pigs and humans, while peptide YY in pigs is ten to twenty times higher and ghrelin two to five times lower than in humans. Pigs are an excellent model for human studies for vagal nerve function related to the hormonal regulation of food intake. Similarly, the study of gut barrier functions reveals conserved defence mechanisms between the two species particularly in functional permeability. However, human data are scant for some of the defence systems and nutritional programming. The pig model has been valuable for studying the changes in human microbiota following nutritional interventions. In particular, the use of human flora-associated pigs is a useful model for infants, but the long-term stability of the implanted human microbiota in pigs remains to be investigated. The similarity of the pig and human brain anatomy and development is paradigmatic. Brain explorations and therapies described in pig, when compared with available human data, highlight their value in nutritional neuroscience, particularly regarding functional neuroimaging techniques.

Dietary peptides are absorbed along the intestine through peptide transporter 1 (PepT-1) which is highly responsive to dietary protein level. PepT-1 is also involved in gut homeostasis, both initiating and resolving inflammation. Low-birth-weight (LBW) neonates are routinely fed a high-protein (HP) formula to enhance growth. However, the influence of this nutritional practice on PepT-1 activity is unknown. Intestinal PepT-1 activity was compared in normal-birth-weight (NBW) and LBW piglets. The effect of HP v. normal-protein (NP) formula feeding on PepT-1 activity and gut homeostasis in LBW piglets was evaluated, during the neonatal period and in adulthood. Flux of cephalexin (CFX) across the tissue mounted in Ussing chambers was used as an indicator of PepT-1 activity. CFX flux was greater in the ileum, but not jejunum or colon, of LBW than NBW piglets during the neonatal period. When LBW piglets were formula-fed, the HP formula increased colonic CFX during the 1st week of life. Later in life, intestinal CFX fluxes and barrier function were similar whether LBW pigs had been fed NP or HP formula. However, colonic permeability of HP- but not NP-fed pigs increased when luminal pH was brought to 6·0. The formyl peptide N-formyl methionyl-leucyl-phenylalanine conferred colonic barrier protection in HP-fed piglets. Heat shock protein 27 levels in the colonic mucosa of HP-fed LBW pigs correlated with the magnitude of response to the acidic challenge. In conclusion, feeding a HP formula enhanced colonic PepT-1 activity in LBW pig neonates and increased sensitivity of the colon to luminal stress in adulthood.

The impact of dietary factors on the gut morphological maturation is poorly documented in rabbits. The weights of the digestive segments as well as the morphology of villi and crypts along the small intestine were analysed weekly from day 14 till day 49, in two rabbit groups weaned at either 21 (W21 group, n = 12 litters) or 35 days (W35 group, n = 12 litters) of age. From 21 till 35 days, the W21 group ate 57% more solid feed than the W35 group (P < 0.01), and presented slighter body weights from day 28 till day 49 (-9%, P < 0.05). Tissue weights of the empty digestive segments, as expressed relative to the body weights, were higher in the W21 than in the W35 group from day 28 till day 49 (P < 0.001), whereas absolute tissue weights appeared similar (except for the proximal colon). From day 28 to day 49, small intestinal villi grew in height and surface area (P < 0.05) whereas the crypts deepened. Villous height followed a proximo-distal decreasing gradient from the duodenum to the ileum (P < 0.05) from day 28 onward. The villous height to width ratio changed with the beginning of significant solid feed intake: from a thin shape until day 21, villi became wider from day 28 on. The effect of weaning age on mucosal morphology was insignificant, except for the jejunal crypts whose surface area and depth were higher in the W21 group. The present results showed that morphological changes in the digestive tract of young rabbits were weakly influenced by an early stimulation of solid feed intake.

The developmental changes of both pancreatic and intestinal enzymes and the influence of dietary composition on enzyme activities were followed in suckling and weaning rabbits. In addition, whole tract digestibility of nutrients was recorded in response to two dietary energetic sources. Rabbits were fed ad libitum either a low fat and high starch diet (group LF), or a high fat and high fibre diet (group HF) between d 32 and d 42, with both groups receiving a growing finishing diet thereafter. Before weaning (d 32) nutrient digestion was high (>75% for organic matter, protein or fat), and then decreased sharply, except for fat. Between d 32 and d 42, digestion in the HF group was 7.5 and 4.6% lower, respectively, for organic matter and protein, while fibre and fat digestion was higher (+14.0 and +5.0%, respectively). Between d 25 and d 42 of age, pancreatic-specific activities of trypsin and chymotrypsin did not change while those of amylase and lipase increased by 1.5- and 76- fold (P<0.05), respectively. However, total activities and relative activities expressed on a LW basis were increased after weaning as a main consequence of a specific increased organ weight and pancreatic protein content. Relative activities of trypsin and chymotrypsin increased by 63 and 56% (P<0.01) after weaning, respectively. Total activities of pancreatic enzymes measured in the total small intestinal contents increased during the same period, but the range of variations was lower than those measured in the pancreatic gland. Total activities of lipase, trypsin and chymotrypsin measured in the small intestine contents were significantly correlated with pancreas enzyme potentialities. Total small intestine activity of lipase was 58% higher (P<0.001) in HF than in LF group while the other pancreatic and intestinal enzyme activities measured were not influenced by the energetic sources of the diet. Decreased digestibility of organic matter and protein observed with the HF diet could not be related to changes in pancreatic or intestinal enzymatic profiles and may be more dependent on quality of dietary ingredients.

Glucagon-like peptide 2 (GLP-2) may mediate in part the rapid growth effects of luminal nutrients in the small intestine of newborns. The objectives of this study were to determine plasma GLP-2 concentrations and small intestinal GLP-2 receptor (GLP-2R) mRNA abundance (measured by reverse transcription polymerase chain reaction) during pre- and postnatal development and the relationship between these variables and small intestinal growth in enterally and parenterally fed fetal and newborn pigs (premature and term-delivered, 92 and 100% gestation, respectively). Plasma GLP-2 concentrations increased before birth, peaked in suckling 1-d-old pigs (87 +/- 14 pmol/L, P < 0.05), decreased with weaning-related anorexia (34 +/- 5 pmol/L, P < 0.05) and increased when normal food intake resumed (81 +/- 9 pmol/L, P < 0.05). Plasma GLP-2 concentrations were increased 1 d after enteral infusion of colostrum in fetal pigs at 92% gestation compared with untreated controls (59 +/- 11 vs. 7 +/- 2 pmol/L, P < 0.05). In newborn pigs, plasma GLP-2 was increased 2-6 d after the enteral administration of a milk diet, compared with the parenteral infusion of elemental nutrients, but the time course of the response was delayed in premature newborn pigs. Small intestinal GLP-2R mRNA abundance was highest at birth and decreased with enteral food intake in fetal, suckling and weaned pigs (P < 0.05). In contrast, enteral feeding increased (P < 0.05) relative small intestinal weight and/or villous heights in these pigs. We conclude that the introduction of enteral feeding transiently increases plasma GLP-2 concentrations and decreases small intestinal GLP-2R mRNA levels during pig development. GLP-2 may play a role in the growth of the small intestine around birth and weaning via a response to enteral nutrition.

We have cloned the calf predominant pancreatic cholecystokinin B (CCKB)/gastrin receptor cDNA. It encodes a 454 amino acid protein with 90% identity with the CCKB/gastrin receptor cloned in other species and tissues. However, the calf pancreatic CCKB/gastrin receptor contains a pentapeptide cassette within the third intracellular loop which is absent in the cloned human brain and stomach receptor. Quantification of the CCKB/gastrin receptor mRNA levels by reverse transcription polymerase chain reaction demonstrated the same level of transcripts at birth, +7 and +28 days. On the other hand, binding study with pancreatic membranes showing a dramatic increase (600-fold) in the number of CCKB/gastrin receptor sites between at birth and +28 days indicates that the development of the calf pancreatic CCKB/gastrin receptor occurs during the first 4 weeks of post-natal life. COS monkey cells (COS-7 cells) transiently transfected by the cloned cDNA exhibit binding of 125I-Bolton-Hunter-[Thr28,Ahx31]CCK-(25-33) and 125I-Bolton-Hunter-[Leu15]human gastrin-(2-17) to two affinity classes of sites. Kd values of the high affinity binding components indicate a 4-fold higher affinity of the receptor for sulfated gastrin than for CCK. Finally, the recombinant receptor is coupled to G proteins and [Ca2+]i mobilization, and is expressed as a glycoprotein of 82 kDa.

Changes in the activities of three gastric and nine pancreatic enzymes plus colipase were determined during postnatal development and weaning in calves. In calves exclusively milk-fed for 2, 7, 28, 56, 70 and 119 d, the enzyme activities per kilogram of empty live weight increased with age for chymotrypsin, elastase, carboxypeptidases A and B, ribonuclease and alpha-amylase, decreased for chymosin, lysozyme and colipase but showed no change in the case of pepsin, trypsin, lipase and phospholipase A2 compared with animals at birth. The greatest increase was that in alpha-amylase activity (about 50-fold between d 2 and 119). In calves weaned between d 28 and 56, all the activities were higher than in milk-fed animals, except that of chymosin (which was slightly lower) and that of colipase (which did not change). At 119 d of age, chymotrypsin, carboxypeptidase A, alpha-amylase and lipase were 1.6- to fourfold higher in ruminants than in preruminants. Thus, most enzyme activities were modified first by colostrum and milk intake, and again upon weaning by development of the forestomachs and ingestion of solid food. These ontogenic patterns might be under the control of many gut regulatory peptides, the plasma concentrations of which changed simultaneously. Some gastric and pancreatic enzymes were correlated to plasma concentrations of these gut regulatory peptides.