Small Intestinal Growth Research Articles

Effects of soybean agglutinin on nitrogen metabolism and on characteristics of intestinal tissues and pancreas in rats

Two experiments were conducted to investigate the effects of increasing concentrations of supplemental purified soybean agglutinin on performance, apparent nitrogen digestibility, plasma insulin and cholecystokinine (CCK) levels in rats as well as on the growth of the small intestine and pancreas. In Experiment 1, a 10-day nitrogen balance trial was conducted with 24 male Sprague-Dawley rats (mean BW 85 g) that were randomly allotted to one of four dietary treatments. Rats in each group were provided daily with 7 g of a casein-cornstarch based diet (control) or a diet supplemented with purified soybean agglutinin at 0.4, 0.6 or 0.8 mg/g. Urine and faeces were collected daily and stored at − 20°C until analysis. In Experiment 2, 30 male Sprague-Dawley rats (mean BW 75 g) were divided into five groups for a 20-day growth experiment. Each rat was fed daily 7 g of a casein-cornstarch based diet (control) or a diet supplemented with purified soybean agglutinin at 0.4, 0.8, 1.2 or 2.0 mg/g. All experimental diets were adjusted to contain a similar level of nutrients. Results from the two experiments showed that supplementation of soybean agglutinin below 2.0 mg/g diet had no significant effect on rat performance. However, rats receiving 2.0 mg soybean agglutinin per gram of diet showed a significant reduction in weight gain compared to the control group. Incorporation of soybean agglutinin in the diet reduced apparent nitrogen digestibility and the retention of dietary nitrogen by increasing nitrogen loss from the faeces and urine. In addition, plasma CCK level increased with increasing inclusion of soybean agglutinin in the diet. On the contrary, the plasma insulin level declined as soybean agglutinin level increased. Soybean agglutinin induced a polyamine-dependent hyperplastic and hypertrophic growth of the small intestine and pancreas by increasing the contents of protein, RNA and DNA, though the increase in weight of small intestine was not significant. Furthermore, 1.2 and 2.0 mg soybean agglutinin per gram of diet promoted proliferation of the jejunum mucosa, while the structure of the brush border epithelium of small intestinal had no damaging change and no diarrhoea was observed in any treatment group. Based on these results, supplementation of low doses of soybean agglutinin or soy protein to parenterally-fed animals affected by atrophic small intestine may promote small intestinal growth.

Dietary protein hydrolysates vs. the intact proteins do not enhance mucosal integrity and growth performance in weaned piglets

Two separate experiments, but using the same diets, were designed to study whether the addition to the diet of protein hydrolysates or crystalline glutamine (gln) affect small intestinal integrity (experiment 1) and growth performance (experiment 2). It was hypothesized that dietary supplementation of hydrolysed proteins would increase the availability of amino acids for the gut wall and therefore result in an improved small intestinal integrity and growth performance of piglets after weaning. The five diets differed in their protein composition: soybean meal and wheat gluten (SBM+WG), SBM and hydrolysed wheat gluten (SBM +HWG), hydrolysed soybean meal and WG (HSBM+WG), SBM and potato protein (SBM+PP), 2% of gln added to SBM and PP (SBM+PP+gln). In experiment 1, 88 piglets of 8.4 kg (S.D.: 0.82) were weaned at 26 days of age (day 0). Piglets were dissected and sampled on days 0, 3, or 7 postweaning. Results showed that the protein hydrolysates did not increase villus height, did not reduce crypt depth and did not raise brush-border aminopeptidase and isomaltase–sucrase activity when compared to the diets containing the unhydrolysed proteins. In experiment 2, 165 piglets of 8.5 kg (S.D.: 1.33) were weaned at 26 days of age. Feed intake and weight gain were not enhanced by the protein hydrolysates. The addition to the diet of crystalline gln resulted in improved average daily gain and feed efficiency by 22 and 17%, respectively ( P<0.05) when compared to the other diets and measured during the first 2 weeks postweaning. Gln did not influence growth performance during days 0–7 postweaning. The feeding of protein hydrolysates led to more non-consistent faeces when compared to the SBM+WG diet ( P<0.05). In conclusion, dietary supplementation of protein hydrolysates did not ameliorate the weaning-induced compromise of small intestinal integrity and did not enhance growth performance. Dietary supplementation of gln did not affect villus architecture during the 1st week postweaning, but it enhanced growth performance during the 2nd week.

Glucagon-like peptide-2 receptor activation in the rat intestinal mucosa.

Glucagon-like peptide-2 (GLP-2) increases small intestinal growth and function in rodents and human subjects. GLP-2 exerts its effects through a seven-transmembrane domain, G protein-coupled receptor (GLP-2R), stimulating cAMP generation and activating protein kinase A signaling in heterologous cell lines transfected with the GLP-2R. As intestinal cell lines expressing the GLP-2R have not been identified, we developed methods for studying GLP-2R signaling in the rat small intestinal mucosa in vitro. Isolated rat intestinal mucosal cells expressed mRNA transcripts for the GLP-2R, as well as for chromogranin A and beta-tubulin III, markers for enteroendocrine and neural cells, respectively. cAMP production in response to [Gly2]GLP-2, a degradation-resistant analog of GLP-2, was maximal at 10-11 m (268 +/- 93% of control, P < 0.001), with reduced cAMP accumulation observed at higher doses. The cAMP response was diminished by pretreatment with 10-9 m GLP-2, and was abolished by pretreatment with 10-6 m GLP-2 (P < 0.05), indicating receptor desensitization. GLP-2 treatment of isolated mucosal cells increased 3H-thymidine incorporation (to 128 +/- 8% of controls, P < 0.05), and this was prevented by inhibition of the protein kinase A pathway with H89. In contrast, GLP-2 did not affect p44/p42 MAPK phosphorylation or the levels of cytosolic calcium in the mucosal cell preparation. These results provide the first evidence that activation of the endogenous rat mucosal GLP-2 receptor is linked to activation of a cAMP/protein kinase A-dependent, growth-promoting pathway in vitro.

Introduction of Enteral Food Increases Plasma GLP-2 and Decreases GLP-2 Receptor mRNA Abundance during Pig Development

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.

Minimal Enteral Feeding Induces Maturation of Intestinal Motor Function but Not Mucosal Growth in Neonatal Dogs

Providing small enteral feedings for parenterally fed preterm infants during the first few weeks of life improves feeding tolerance. However, it is not known whether these feedings achieve this result via stimulation of gut growth and/or maturation of function. The minimal level needed to attain these responses is also critical to identify, because neonatologists often limit feeding volumes to minimize the risk of necrotizing enterocolitis. Thus, we determined the dose-response relationships between enteral feeding volume and gastrointestinal growth and small intestine motor function. Newborn canine pups (n = 51) received 0, 2.5, 5.0, 7.5, 10, 30 or 100% of their daily fluid intake enterally with the remainder given parenterally for 4-5 d. Motor activity was recorded, blood drawn for determination of gastrin and motilin, and intestinal tissue harvested for determination of DNA and protein content and morphology. Feeding volumes that provided 30% or more of daily fluid intake significantly increased small intestinal mucosal growth above that of unfed pups, but feeding volumes that provided as little as 10% of daily fluid intake significantly induced maturation of motor patterns beyond that of unfed pups. Plasma concentrations of gastrin and motilin did not differ among groups. We conclude that small enteral feedings typically used for minimal enteral feeding strategies improve feeding tolerance by triggering maturation of motor function but not gut growth in neonatal dogs. Small feeding volumes trigger this maturation as well as large volumes.

Small intestine growth and morphometry in piglets weaned at 7 days of age. effects of level of energy intake.

Two trials involving a total of 56 pigs were conducted to examine the effects of weaning at 7 d of age (trial 1) and of energy intake level and length of post-weaning underfeeding period (trial 2) on small intestinal (SI) development and morphometry. At 3 d after weaning, weight of the SI and mucosa (g/kg body weight) and villous height along SI were reduced by 20, 36 and 41%, respectively, compared to the day of weaning. Intestinal morphometrical changes are dependent on SI site and days post-weaning. Villous atrophy on d 3 and recovery on d 14 post-weaning were greater and occurred earlier in the proximal than in the medial and distal SI. Villous height was dependent on the level of energy intake which explains 56% of the variations in proximal SI villous height in weaned pigs and 73% when data of the sow-reared pigs were included in the analysis. Moreover, after 4 d of refeeding, underfed piglets showed similar villous characteristics to piglets fed a continuously high feeding level after weaning stressing that capacities of intestinal restoration were not affected by the length of the post-weaning underfeeding period. Overall, the present results suggest a spatial and temporal effect of weaning on villous atrophy and recovery, and that the level of energy intake is a major factor accounting for the post-weaning villous height.

Contribution of gastrin-releasing peptide and its receptor to villus development in the murine and human gastrointestinal tract

Recent studies have shown that aberrantly expressed gastrin-releasing peptide (GRP) and its receptor (GRP-R) critically regulate tumor cell differentiation in colon cancers developing in humans and mice. This finding suggested that the ability of GRP/GRP-R to promote a well-differentiated phenotype in colon cancer might reflect a re-capitulation of a normal role in regulating intestinal organogenesis. To determine if this was the case, we compared and contrasted intestinal development in GRPR −/− mice with their wild type littermates. GRP/GRP-R co-expression in wild type mice was only observed in villous enterocytes between N-1 and N-12. During this time frame villous growth was completely attenuated in GRPR −/− mice. The contribution of GRP/GRP-R to villous growth was due to their act in increasing enterocyte proliferation prior to N-8 but increasing enterocyte size thereafter. From N-12 onwards, small intestinal villous growth in GRPR −/− mice resumed such that no difference in this structure could be detected at adulthood between mice of either genotype. We next studied GRP/GRP-R expression in human abortuses. These proteins were co-expressed by villous enterocytes only between weeks 14 and 20 post-conception, a time frame analogous to when they are expressed in the murine intestine. Thus, this study shows for the first time that GRP/GRP-R play a transient and non-critical role in intestinal development, yet provides a rationale for their re-appearance in colon cancer.

GLP-2 has differential effects on small intestine growth and function in fetal and neonatal pigs

Glucagon-like peptide-2 (GLP-2) is a potent intestinotropic factor in neonatal and adult animals. However, the GLP-2 responsiveness of the fetal intestine has not been established. To determine how stage of development affects the responsiveness to GLP-2, we examined GLP-2 receptor (GLP-2R) expression, gut morphology, and brush-border enzyme mRNA and activities in late-gestation fetal (n = 7) and parenterally fed neonatal (n = 7) piglets given GLP-2 (12.5 nmol/kg) twice daily for 6 days. The GLP-2R was expressed in the fetal and neonatal gastrointestinal tract. The biologically active GLP-2-(1-33) was undetectable (<5 pmol/l) in plasma of 98-day-gestation fetuses but increased significantly toward full term (115 days, 11 +/- 1 pmol/l) and in neonates fed by total parenteral nutrition (23 +/- 5 pmol/l). Exogenous GLP-2 had no effect on gut growth in fetuses but increased intestinal weight and villus height in neonates (P < 0.05). Crypt cell proliferation and the enzymes sucrase-isomaltase, lactase-phloridzin hydrolase, aminopeptidase A, and dipeptidyl peptidase IV were unchanged by GLP-2 in both groups. Aminopeptidase N mRNA and activity were increased in fetuses, while maltase mRNA and activity were increased in neonates. In conclusion, exogenous GLP-2 had different effects on small intestine growth and function in fetuses and neonates. This may be related to the normal developmental changes in intestine growth and function and to a maturation of the GLP-2R signaling pathways around the time of birth.

Increasing viscosity of the intestinal contents alters small intestinal structure and intestinal growth, and stimulates proliferation of enterotoxigenicEscherichia coliin newly-weaned pigs

Sources of viscous soluble fibre, such as barley and oats, have often been included in the weaning diet of the pig to accelerate development of the large intestine. Inclusion of a non-fermentable, viscous compound, sodium carboxymethylcellulose (CMC), in a low-fibre weaning diet was tested to assess the influence of digesta viscosity on the gut in the absence of increased fermentation. Two CMC sources, of low and high viscosity, were added to cooked rice-based diet at 40 g/kg total diet. A third control rice diet did not contain any CMC. Diets were fed for 13 d following weaning at 3 weeks of age. Addition of CMC to the diet significantly increased the intestinal viscosity of digesta within the small (P<0.001) and large (P<0.05) intestine. No simple association was found between increases in intestinal viscosity and effects on intestinal morphology and whole-body growth. The average empty-body-weight gain and the small intestinal villus height increased with low-viscosity CMC, but decreased with the high-viscosity CMC group. The full large intestinal weight increased in all pigs fed CMC. Dietary CMC (both low- and high-viscosity) increased the percentage moisture of digesta and faeces, and was associated with increased faecal shedding of enterotoxigenic haemolytic Escherichia coli. Feed ingredients in weaning diets that excessively increase the viscosity of the intestinal digesta may be detrimental to pig health and production.

Effect of the Central Nervous System on Mucosal Growth and Apoptosis in the Small Intestine

Recently our studies have demonstrated that the central nervous system regulates in part mucosal cell growth and apoptosis in the rat small intestine. Ornithine decarboxylase (ODC) activity is a key enzyme for polyamine synthesis which plays an important role for the intestinal mucosal growth. We have demonstrated that the increase of ODC activity in the duodenum just before the dark period is abolished by truncal vagotomy and that the infusion of 2-deoxy-D-glucose into the third cerebroventricle activates ODC activity in the small intestine. Epithelial homeostasis is balanced by regulation of cell proliferation and cell death. Our preliminary data showed that intestinal mucosal apoptosis decreased in the ventromedial-hypothalamus-lesioned rat. These results indicate that the central nervous system, in addition to local factors, is related to regulation of mucosal homeostasis in the intestinal mucosa.

Dietary Plasma Protein Reduces Small Intestinal Growth and Lamina Propria Cell Density in Early Weaned Pigs

ABSTRACT We quantified the effects of a diet containing animal plasma protein on small intestinal growth and mucosal morphology in early weaned pigs. Ninety-six pigs [14 d old, 4 kg body weight (BW)] were assigned in groups of 32 to three dietary treatments as follows: 1) free access to control diet (C), 2) free access to plasma protein diet (P), and 3) plasma protein, pair-fed to C (PPF). Eight pigs from each group were killed at 2, 4, 8 or 16 d. Over a 16-d period, weight gain in the P group was 43% greater (P < 0.05) than that in C pigs; weight gain was similar in C and PPF groups. Protein intake in the P group was 33% higher (P < 0.05) than that in the PPF group; no significant difference was observed between the C and P groups. Dietary protein conversion efficiencies in both the P and PPF groups were approximately 18% greater (P < 0.05) than those in the C group. Intestinal masses in the three groups did not differ at 2, 4 and 8 d. By 16 d, the jejunal and ileal protein and DNA masses (mg/kg BW) in both the P and PPF groups were lower than those in the C group (P < 0.05). Dietary plasma protein did not affect crypt cell proliferation, crypt depth or villous height in either the jejunum or ileum. However, the intravillous lamina propria cell density in the jejunum was significantly lower (P < 0.05) in P and PPF pigs than in C pigs. Plasma urea concentrations were also 40 and 42% lower (P < 0.05) in the P and PPF groups, respectively, than in the C group. Our results indicate that dietary plasma protein reduces the cellularity of the lamina propria, but not epithelial cell surface of the small intestine. Feeding plasma protein also increased the efficiency of dietary protein utilization, in part, by decreasing amino acid catabolism.

Keratinocyte growth factor enhances early gut adaptation in a rat model of short bowel syndrome.

To evaluate the effects of keratinocyte growth factor (KGF) on intestinal adaptation after resection of 85% of the small intestine and consider its potential application in short bowel syndrome (SBS). Experimental study using a known model of SBS. Thirty male Sprague Dawley rats. Four groups of animals were designated. Two groups underwent 85% resection of the small intestine, while the other two groups were sham-operated, undergoing transection and reanastomosis. Resected and sham-operated groups then received either 3 mg/kg KGF or vehicle subcutaneously daily for 3 days. Gut adaptation was evaluated by measurements of mucosal cellularity and biochemical activity in duodenal, jejunal, and ileal segments. Significant small intestinal growth after bowel resection alone was confirmed in resected versus sham-operated rats. KGF further augmented this growth in the resected animals. Mucosal wet weight of the small intestine increased with resection and was further increased (by 20% or more) with KGF administration. Mucosal thickness, villus length, and crypt depth exhibited similar patterns of response. The KGF-induced increase in mucosal morphology was accompanied by increased mucosal DNA and protein content, followed by a trend toward increased mucosal enzyme activity. Histology demonstrated an increase in goblet cells in KGF-treated animals. In situ hybridization analysis demonstrated that KGF markedly increased mucosal expression of intestinal trefoil protein (ITF) mRNA. KGF enhances gut growth, differentiation, and gene regulation during adaptation in rat small intestine after massive resection. KGF may be beneficial in the management of veterinary and human patients undergoing massive intestinal resection.

Fetal organ growth in response to oesophageal infusion of amniotic fluid, colostrum, milk or gastrin-releasing peptide: a study in fetal sheep

The hypothesis of the present study was that the infusion of the biological fluids to which the developing gut is normally exposed (i.e. amniotic fluid, colostrum, milk) and a single growth factor (gastrin-releasing peptide), which is found in high concentrations in fetal fluids and milk, could ameliorate the altered growth induced by the elimination of swallowed input secondary to ligation of the oesophagus. At 108-110 days of gestation the fetal oesophagus was ligated and a catheter inserted towards the stomach (32 fetuses). At 117-119 days of gestation saline (n = 5), amniotic fluid (n = 5), colostral whey (n = 5), milk whey (n = 5) or gastrin-releasing peptide (3.6 nmol day(-1), n = 6), was infused for 7 days (4 x 20 mL day(-1)), or no infusion was given (ligated group, n = 6). A further 15 fetuses were not ligated (normal group, n = 15). All fetuses had carotid artery and/or jugular vein catheters implanted. At 124-126 days of gestation the fetus was delivered and fetal body and organ weights recorded. Analysing the results by ANOVA, there were no effects of either ligation alone or infusion after ligation on fetal weight, crown-rump length, or weight relative to bodyweight of heart, adrenal, pancreas, large intestine and cecum. There were significant differences between the infusion groups for lungs, kidney, pancreas, total gut, abomasum, small intestine, spleen, chest and neck thymus, and mesenteric lymph nodes. Ligation alone significantly reduced small intestinal growth and increased kidney and spleen growth. Colostrum infusion enhanced growth of most organs. Gastrin-releasing peptide significantly increased growth of all the immune organs studied. It was concluded that at an age when premature delivery could be encountered, the fetal gut is capable of significant adaptive growth, to varying degrees, depending on the enteral diet. Growth effects in organs distant to the gut suggest that either gastrointestinal uptake and transport of growth factors or altered nutrient uptake and/or availability can affect the growth of other major fetal organs.

Effect of prolonged intraluminal alpha-amylase inhibition on eating, weight, and the small intestine of rats.

Effects of chronic intraluminal amylase inhibition on eating and the digestive system are unclear. In growing rats, we determined the effect of ingesting a wheat amylase inhibitor (AI) on eating, weight, small intestinal mucosal growth, and disaccharidases. Three groups of 12 rats received AI, were pair-fed controls (PFC), or had free access to food (FAC). After measuring food intake and body and stool weight for 21 d, rats were decapitated and the small intestine was divided into four segments. AI and PFC rats had similar food intake, weight gain, and stool output, but these were less than FAC rats (P < 0.005). AI rats ate less (P < 0.001) than PFC during the light cycle and less than FAC rats during darkness. Mucosal DNA and RNA were reduced (P < 0.05) in the upper small intestine of AI and PFC rats compared with FAC rats. Mucosal weight, RNA, and disaccharidase activities were greater (P < 0.01) in the ileum of AI rats compared with PFC and FAC rats. AI alters the amount and pattern of food intake, reduces weight gain, upper small intestinal mucosal weight, protein and DNA, and increases distal small intestinal mucosal weight, RNA, and disaccharidases. AI likely causes these effects by inducing satiety and increasing carbohydrate delivery to the distal intestine.

Dexamethasone inhibits small intestinal growth via increased protein catabolism in neonatal pigs.

Our objective was to determine how dexamethasone (Dex) affects gastrointestinal protein metabolism and growth in neonatal pigs. Two-day-old pigs were given daily subcutaneous injections of either Dex (1 mg/kg body wt, n = 7) or saline (control, n = 6) for 7 days. In vivo protein synthesis was measured after 7 days with a bolus of [3H]phenylalanine. Tissue protein contents were measured in an initial control group of 2-day-old pigs and in control and Dex pigs after 7 days to estimate protein accretion and degradation. In control pigs, the protein accretion in the ileum was nearly sixfold greater than in the jejunum during the 7-day period. Dex nominally altered stomach growth but completely blocked the accretion of protein and DNA in the jejunum and ileum, with reduced villus height in the ileum. Dex increased the fractional protein degradation rate in the ileum (28%) and decreased the absolute protein synthesis rate in the jejunum and ileum by 17 and 21%, respectively. Dex resulted in a 40% lower total intestinal lactase activity compared with controls via reductions in both specific activity and tissue mass, especially in the ileum. Dex significantly decreased the circulating concentrations of insulin-like growth factor (IGF) I and IGF-binding protein (IGFBP)-1, -2, and -3. However, the tissue abundance of the IGF-I receptor in the stomach and ileum was greater in Dex pigs than controls. Our results suggest that Dex significantly inhibits small intestinal growth via both increased degradation and decreased synthesis of protein. Furthermore, the inhibition of intestinal growth resulted in significantly decreased lactose digestive capacity.

Dietary polyamines are essential luminal growth factors for small intestinal and colonic mucosal growth and development

BackgroundPolyamines are essential for cell growth. Dietary and probably gut bacterial derived polyamines contribute significantly to the polyamine body pool.AimsTo evaluate the influence of dietary, luminal polyamines on growth and...

The role of insulin-like growth factors in small intestinal cell growth and development.

IGF-I and IGF-II receptors are expressed in the small intestine of mammalian species, as are the genes to synthesize both peptides. IGF binding proteins are also expressed in the intestine. IGF-I and IGF-II mRNA are highest in fetal and newborn tissues and decrease with age. IGF-I mRNA is present in the adult small intestine, and is associated with the submucosal regions and crypt cells. IGF-I and IGF-II receptor binding to the small intestine is higher in newborn animals and decreases with age. Both receptors are more concentrated in the crypt than villus regions, but IGF-II binding is higher than IGF-I in all regions. IGF-I receptors are associated with the submucosal region of the small intestine, whereas IGF-II receptors are more abundant in the mucosal cells. Administration of IGF-I either orally or by osmotic pump generally has no affect on small intestinal weight or length, but does increase mucosal cellularity. LR3-IGF-I administration by osmotic pump affects the small intestine similarly to IGF-I, although with a higher potency. In the few studies in which IGF-II was administered, increased gut mass was observed in adult rats, but not newborn rats or pigs. Significant effects on mucosal expression of disaccharidases was achieved with either oral or subcutaneous IGF-I or oral IGF-II. Administration of IGF in models of intestinal hypertrophy and atrophy are also reviewed.

Protease inhibitors and lectins in soya beans and effects of aqueous heat-treatment

Protease inhibitor and lectin concentrations and N and lipid levels were evaluated in 27 soya bean samples. All contained trypsin and chymotrypsin inhibiting activity and lectin. Shinano midori, Shinano wasediro, Shinano-oomame and Tsuronoku had high protein contents and average lipid levels, and their lectin and trypsin and chymotrypsin inhibitory activities were not unduly high. These lines, in particular, merit further nutritional evaluation. Food intake, feed conversion efficiency and growth by rats was reduced when soya bean was included in their diet, but the extent to which these parameters were affected did not appear to depend only on the protease inhibitor or lectin content. In contrast, pancreatic and small intestinal growth did seem to reflect the levels of these factors in the diet. Chymotrypsin inhibitor activity in soya bean was more readily abolished by heat-treatment than was trypsin inhibitory activity. Lectin activity was also relatively heat-resistant. However, all of these activities could be abolished by aqueous heat-treatment of fully imbibed seeds at 100°C for 10 min. The effects of a soya diet on pancreas and small intestine weights were also abolished by this pre-treatment, and food intake and nutrient utilisation by rats was greatly improved. © 1998 Society of Chemical Industry

Protease inhibitors and lectins in soya beans and effects of aqueous heat‐treatment

Protease inhibitor and lectin concentrations and N and lipid levels were evaluated in 27 soya bean samples. All contained trypsin and chymotrypsin inhibiting activity and lectin. Shinano midori, Shinano wasediro, Shinano-oomame and Tsuronoku had high protein contents and average lipid levels, and their lectin and trypsin and chymotrypsin inhibitory activities were not unduly high. These lines, in particular, merit further nutritional evaluation. Food intake, feed conversion efficiency and growth by rats was reduced when soya bean was included in their diet, but the extent to which these parameters were affected did not appear to depend only on the protease inhibitor or lectin content. In contrast, pancreatic and small intestinal growth did seem to reflect the levels of these factors in the diet. Chymotrypsin inhibitor activity in soya bean was more readily abolished by heat-treatment than was trypsin inhibitory activity. Lectin activity was also relatively heat-resistant. However, all of these activities could be abolished by aqueous heat-treatment of fully imbibed seeds at 100°C for 10 min. The effects of a soya diet on pancreas and small intestine weights were also abolished by this pre-treatment, and food intake and nutrient utilisation by rats was greatly improved. © 1998 Society of Chemical Industry

Diet Supplemented with Yoghurt or Milk Fermented by Lactobacillus casei DN-114 001 Stimulates Growth and Brush-Border Enzyme Activities in Mouse Small Intestine

The nutritional benefits of lactic acid bacteria in fermented dairy products have been well documented, especially in terms of weight gain and feed efficiency, but not in terms of small intestine adaptation. The effects of a diet supplemented (30% wt/wt) with milk fermented either by Lactobacillus casei DN-114 001 or yoghurt for 3 or 15 days were investigated in the small intestine of mice by morphometry, kinetic analysis and determination of brush-border enzyme activities. Results were compared with those obtained with standard or milk isocaloric diets. Cell proliferation and villous area were significantly increased in the proximal intestine of mice fed the fermented-milk-supplemented diets for 3 days and were associated with hypertrophy and hyperplasia of Paneth and goblet cells. Lactase-specific activity was increased by fermented-milk diets at days 3 and 15, whereas there was no variation in maltase-specific activity. Alkaline phosphatase-specific activity was increased after 3 days of the three tested diets in the whole intestine, and after 15 days in the proximal intestine. Aminopeptidase activity was increased in the distal part of the intestine after 3 days of the 3 diets. Our findings suggest that diets supplemented with fermented milks have a positive effect on the trophicity of the mucosa in the small intestine of mice.