Jejunal Mucosal Surface Area Research Articles

Effect of feeding soybean meal and differently processed peas on intestinal morphology and functional glucose transport in the small intestine of broilers

Peas are locally grown legumes being rich in protein and starch. However, the broad usage of peas as a feed component in poultry nutrition is limited to anti-nutritional factors, which might impair gut morphology and function. This study investigated the effect of feeding raw or differently processed peas compared with feeding a soybean meal-based control diet (C) on intestinal morphology and nutrient transport in broilers. A total of 360 day-old broiler chicks were fed with one of the following diets: The C diet, and 3 diets containing raw peas (RP), fermented peas (FP) and enzymatically pre-digested peas (EP), each supplying 30% of dietary crude protein. After 35 d, jejunal samples of broilers were taken for analyzing histomorphological parameters, active glucose transport in Ussing chambers and the expression of genes related to glucose absorption, intestinal permeability and cell maturation. Villus length (P = 0.017) and crypt depth (P = 0.009) of EP-fed broilers were shorter compared to birds received C. The villus surface area was larger in broilers fed C compared to those fed with the pea-containing feed (P = 0.005). Glucose transport was higher for broilers fed C in comparison to birds fed with the EP diet (P = 0.044). The sodium-dependent glucose co-transporter 1 (SGLT-1) expression was down-regulated in RP (P = 0.028) and FP (P = 0.015) fed broilers. Correlation analyses show that jejunal villus length negatively correlates with the previously published number of jejunal intraepithelial T cells (P = 0.014) and that jejunal glucose transport was negatively correlated with the occurrence of jejunal intraepithelial leukocytes (P = 0.041). To conclude, the feeding of raw and processed pea containing diets compared to a soybean based diet reduced the jejunal mucosal surface area of broilers, which on average was accompanied by lower glucose transport capacities. These morphological and functional alterations were associated with observed mucosal immune reactions. Further studies are required elucidating the specific components in peas provoking such effects and whether these effects have a beneficial or detrimental impact on gut function and animal health.

Effects of exogenous glucagon-like peptide-2 and distal bowel resection on intestinal and systemic adaptive responses in rats.

ObjectiveTo determine the effects of exogenous glucagon-like peptide-2 (GLP-2), with or without massive distal bowel resection, on adaptation of jejunal mucosa, enteric neurons, gut hormones and tissue reserves in rats.BackgroundGLP-2 is a gut hormone known to be trophic for small bowel mucosa, and to mimic intestinal adaptation in short bowel syndrome (SBS). However, the effects of exogenous GLP-2 and SBS on enteric neurons are unclear.MethodsSprague Dawley rats were randomized to four treatments: Transected Bowel (TB) (n = 8), TB + GLP-2 (2.5 nmol/kg/h, n = 8), SBS (n = 5), or SBS + GLP-2 (2.5 nmol/kg/h, n = 9). SBS groups underwent a 60% jejunoileal resection with cecectomy and jejunocolic anastomosis. All rats were maintained on parenteral nutrition for 7 d. Parameters measured included gut morphometry, qPCR for hexose transporter (SGLT-1, GLUT-2, GLUT-5) and GLP-2 receptor mRNA, whole mount immunohistochemistry for neurons (HuC/D, VIP, nNOS), plasma glucose, gut hormones, and body composition.ResultsResection increased the proportion of nNOS immunopositive myenteric neurons, intestinal muscularis propria thickness and crypt cell proliferation, which were not recapitulated by GLP-2 therapy. Exogenous GLP-2 increased jejunal mucosal surface area without affecting enteric VIP or nNOS neuronal immunopositivity, attenuated resection-induced reductions in jejunal hexose transporter abundance (SGLT-1, GLUT-2), increased plasma amylin and decreased peptide YY concentrations. Exogenous GLP-2 attenuated resection-induced increases in blood glucose and body fat loss.ConclusionsExogenous GLP-2 stimulates jejunal adaptation independent of enteric neuronal VIP or nNOS changes, and has divergent effects on plasma amylin and peptide YY concentrations. The novel ability of exogenous GLP-2 to modulate resection-induced changes in peripheral glucose and lipid reserves may be important in understanding the whole-body response following intestinal resection, and is worthy of further study.

PP261-SUN: Outstanding abstract: Calorie Requirements of Chronically Ventilated, Brain Impaired Children

and circumference (10.7±0.9mm vs. NS 8.5±0.9mm and LCT 9.0±0.9mm, p < 0.001). Although there were no differences in jejunal length, villus height, villus width or crypt width, mucosal-to-serosal amplification ratio calculations revealed greater jejunal mucosal surface area with MCT (327±77cm2 vs. NS 193±85cm2 and LCT 215±40cm2, p < 0.01). Conclusion: MCT appear superior to NS and LCT in increasing jejunal gross morphology and mucosal surface area after massive ileocecal resection, independent of enteric hormones. It remains to be determined whether MCT can stimulate functional adaptation of remnant jejunum in SBS.

PP262-SUN: The Role of Interleukin-6 Gene 572 G/C Polymorphism in Child Obesity

and circumference (10.7±0.9mm vs. NS 8.5±0.9mm and LCT 9.0±0.9mm, p < 0.001). Although there were no differences in jejunal length, villus height, villus width or crypt width, mucosal-to-serosal amplification ratio calculations revealed greater jejunal mucosal surface area with MCT (327±77cm2 vs. NS 193±85cm2 and LCT 215±40cm2, p < 0.01). Conclusion: MCT appear superior to NS and LCT in increasing jejunal gross morphology and mucosal surface area after massive ileocecal resection, independent of enteric hormones. It remains to be determined whether MCT can stimulate functional adaptation of remnant jejunum in SBS.

Expression of tight-junction proteins in human proximal small intestinal mucosa before and after Roux-en-Y gastric bypass surgery

BackgroundIncreased permeability and uptake of proinflammatory bacterial endotoxins from gut microbiota has been suggested as a mechanism for obesity-associated chronic inflammation that causes obesity-associated insulin resistance. We hypothesized that intestinal barrier function may be restored after Roux-en-Y gastric bypass (RYGB) surgery and thereby contribute to decreased inflammation. The objective of this study was to investigate levels of the permeability-regulating tight-junction proteins in human small intestinal mucosa before and after RYGB surgery. MethodsPaired intraindividual jejunal mucosa samples were retrieved at the time of surgery and 6 to 8 months after surgery. Mucosal cell surface area was calculated by histomorphometry. Mucosal samples were analyzed by proteomics to find patterns of protein regulations. Based on these findings further analyses were performed by Western blotting. Ussing chambers were used to analyze permeability in the retrieved mucosal samples. ResultsMucosal surface area was significantly decreased after surgery. Global protein expression analysis showed a significant increase in the cytokeratin-8 (Ck8), which was confirmed by Western blotting. Further analyses showed a significant increase in claudin-3 and -4 expression after surgery, whereas occludin and zonula occludens-1 levels were decreased. Expressions of claudin-1, -2, -5 and vinculin were unchanged. Ussing chamber experiments revealed a linear correlation between the epithelial electrical resistance and claudin-3 protein expression. ConclusionSeveral alterations were found in the rerouted small intestine after surgery, indicating a decreased jejunal mucosal surface area and decreased paracellular permeability. These changes could contribute to decreased uptake of luminal microbiota-derived inflammatory mediators such as endotoxins after RYGB.

Feeding diets containing 2% cheno- or urso-deoxycholic acid or cholestyramine to rats for two weeks alters intestinal morphology and bile acid absorption

This study was undertaken to examine the effect of supplementing chow for 2 weeks with 2% cheno- (CDC) or ursodeoxycholic (UDC) acid or cholestyramine (CHOL) on the intestinal morphology and in vitro uptake of bile acids in adult rats. Food intake was higher in UDC and CHOL as compared with animals fed chow or CDC, or in animals pair-fed a chow-restricted diet (CRD). Body weight gain was lower in CDC and CRD but was unchanged by feeding UDC or CHOL. Jejunal mucosal surface area was similar in the five groups, although the ileal mucosal surface area was lower in UDC than in the other animals. Feeding UDC reduced the ileal uptake of cholic acid (C), taurocholic acid (TC), and glycocholic acid (GC). Feeding CDC had no effect on bile acid uptake except when compared with animals fed a chow-restricted diet. Feeding CHOL reduced the active ileal uptake of C, had no effect on the uptake of TC or GC or CDC, and was associated with increased uptake of stearic, linoleic, and linolenic acids. These effects were likely related to a direct effect of changes in the luminal bile acids rather than due to an indirect effect of the reduced food intake, since the ileal uptake of CDC and GC was greater in animals fed CDC than in those fed a chow-restricted diet with comparable weight gain. Thus, 2 weeks of feeding bile acids or bile acid binding agents may alter the form and function of the rat intestine, and as well may lead to changes in food intake and body weight gain.

Fish oil prevents effect of high cholesterol diet on active intestinal transport of galactose.

We tested the hypothesis that diets containing fish oils prevent the effects of a high cholesterol diet on the morphology and nutrient uptake of the intestine. Isocaloric semisynthetic diets were supplemented with beef tallow or fish oil containing low or high amounts of cholesterol and were fed to growing female Wistar rats for 14 days, after which the in vitro jejunal and ileal uptake of glucose, galactose, long-chain fatty acids, and cholesterol was determined. Feeding cholesterol with beef tallow was associated with a 12% decrease in the jejunal mucosal surface area. Feeding fish oil decreased jejunal mucosal surface area by 24%, as compared with the beef tallow diet, but the reduction was increased to 42% when fish oil and cholesterol were fed together. Ileal surface area was unaffected by varying the major source of dietary lipid, or by adding cholesterol. Despite the effect of fish oil on the mucosal surface area, the jejunal and ileal uptake of saturated as well as unsaturated long-chain fatty acids and cholesterol was similar in the four diet groups. Cholesterol supplementation enhanced the jejunal uptake of high concentrations of galactose only when fed with beef tallow, i.e., feeding fish oil prevented the enhancing effect of cholesterol on galactose uptake observed when beef tallow was fed. Thus, (i) a fish oil diet prevents the enhancing effect of cholesterol on jejunal active transport of galactose, an effect not explained by the reduction in jejunal mucosal surface area observed with the fish oil diet; (ii) these dietary manipulations result in a clear dissociation of the morphological from the transport adaptation of the intestine; and (iii) substitution of fish oil for beef tallow as the major source of lipid in the diet prevents the influence of cholesterol on the active intestinal transport of galactose.

Xylose transport in the human jejunum

D-Xylose transport in the human jejunum was studied in vivo using a standard intestinal perfusion technique, and also in vitro in human jejunal brush border membrane vesicles. Initial D-xylose concentrations were linearly related to D-xylose absorption rates, a finding consistent with passive diffusion. Perfusion of D-xylose with varying D-glucose concentrations were aimed at examining D-xylose-D-glucose jejunal cotransport. D-Xylose absorption rates from a 30 mM D-xylose perfusate did not change significantly when 10, 30, or 60 mM glucose were added (-3.0 +/- 0.62 vs -3.34 +/- 0.71, -3.82 +/- 0.81, and -4.56 +/- 0.72 mM/30 cm/hr, respectively; minus indicates net absorption) suggesting an absence of a cotransport system. In brush border membrane vesicles, xylose uptake was partially inhibited by D-glucose and phlorizin. These data suggest that jejunal D-xylose absorption, at concentrations used clinically, is by passive diffusion, which process completely overrides a minor D-glucose cotransport component. The D-xylose tolerance test, therefore, reflects jejunal mucosal surface area and mucosal permeability to D-xylose and not nutrient carbohydrate absorption.

Development of active and passive transport of bile acids in rabbit intestine

Previous studies have indicated that saturable, Na +-bile acid coupled transport is absent in the ileum throughout most of the suckling period and that the maturation of ileal bile acid uptake which occurs during weaning results primarily through an increase in functional bile acid carriers within the ileal brush border membrane. This study was undertaken in weanling and adult rabbits to establish the effect of maturation on the active ileal and passive jejunal and colonic uptake of 8 bile acids. The in vitro uptake of a range of concentrations of cholic (C), taurocholic (TC), glycocholic (GC), chenodeoxycholic (CDC), taurochenodeoxycholic (TCDC), glychochenodeoxycholic (GCDC), deoxycholic (DC) and taurodeoxycholic (TDC) acid was determined. Active ileal uptake of C, TC, GC, DC and TDC was greater in adult that in weanling animals, whereas uptake of CDC, TCDC and GCDC was similar in both groups. The relative permeability for passive uptake of bile acids into the jejunum and colon was similar in young and adult rabbits. Jejunal mucosal surface area was similar in the two groups, but was greater in the ileum in the adult than in the weanling rabbits due to an increase in villus height, width, and number of villi per unit serosal length. However, the age-associated differences in active bile acid uptake were not explained simply on the basis of these differences in ileal mucosal surface area or the concentration of bile acids in the intestinal lumen. Thus, maturation of the rabbit from weanling to adulthood does not influence the relative passive permeability of the jejunum or colon to bile acids, but does increase active ileal uptake of conjugated and unconjugated cholic acid and deoxycholic acid, but not chenodeoxycholic acid

A high linoleic acid diet diminishes enhanced intestinal uptake of sugars in diabetic rats.

Intestinal absorption is altered in rats by diabetes and by dietary manipulation. For 5 wk rats were fed chow (C) or semisynthetic diets containing isocaloric amounts of a high content of either polyunsaturated (P) or saturated (S) fatty acids; then half were rendered hyperglycemic with streptozotocin while the remaining half served as nondiabetic controls. Studies were performed after a total of 8 wk on C, P, or S. Jejunal villous surface area was greater in diabetic rats than in control rats fed C or S, whereas the jejunal mucosal surface area was significantly greater in diabetic animals than in control animals only when they were fed S. Ileal mucosal surface area was similar in diabetic and in control rats fed C, S, or P; although ileal villous surface area was greater in diabetic than in control rats only when they were fed C. The jejunal and ileal uptake of varying concentrations of glucose and galactose was higher in diabetic rats than controls fed C or S. In contrast, the enhanced uptake of these sugars was reduced or normalized in diabetic rats fed P. The jejunal brush-border membrane (BBM) content of phospholipids was higher in diabetic than in control rats fed chow, but there was no difference in diabetic vs. control animals fed P or S in BBM total free fatty acids, phospholipids, or cholesterol. Thus feeding a high linoleic acid diet diminishes the enhanced intestinal uptake of glucose and galactose in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Feeding rats diets containing cheno- or ursodeoxycholic acid or cholestyramine modifies intestinal uptake of glucose and lipids.

We wished to test the hypothesis that variations in the luminal content of bile acid produced by feeding chenodeoxycholic acid (CDC), ursodeoxycholic acid (UDC) or cholestyramine (C) alter intestinal transport properties and morphology. Rats were fed standard chow pellets containing 0.5% CDC, 0.5% UDC or 2% C for a period of 2 weeks, and the in vitro uptake of glucose, cholesterol, bile acids and a homologous series of fatty acids was assessed. The food consumption was similar in animals fed chow, CDC, UDC and C, yet rats fed CDC or UDC gained less weight, and the weight of the jejunal and ileal mucosa was lower in animals fed CDC or C than in those fed chow or UDC. Ileal but not jejunal uptake of glucose was reduced in animals fed UDC, CDC or C. The active ileal uptake of bile acids was enhanced by UDC, CDC or C, whereas the jejunal passive permeability to bile acids was reduced by feeding C. Feeding C inhibited the jejunal and ileal uptake of cholesterol; C, UDC and CDC had a variable effect on the intestinal uptake of the fatty acids 10:0-18:0. The jejunal mucosal surface area was lower in groups fed CDC or UDC as compared with rats fed chow or C, and the ileal mucosal surface area was lower in rats fed CDC. However, the altered intestinal transport could not be explained by the altered morphology. Thus, (1) chronic variations in the intestinal luminal content of bile acids produced by the feeding of CDC, UDC or C resulted in alterations in the active and passive transport properties of the intestine, and (2) these changes differed between the jejunum and the ileum and were not explained simply by alterations in the animals' food intake or mucosal morphology. These studies suggest that chronic variations in the bile acids in the intestinal lumen may be one of the factors independently influencing the transport properties and mucosal surface area of the intestine. The long-term effect of changes in luminal bile acid content on intestinal function in man remains to be established.

Enzymatic and morphometric evidence for Crohn's disease as a diffuse lesion of the gastrointestinal tract.

Intestinal disaccharidase and dipeptidase activities were measured in mucosal biopsies from the proximal jejunum in 20 patients with Crohn's disease apparently confined to the distal ileum or large bowel, 14 patients with ulcerative colitis, and 14 healthy volunteers who acted as controls. The dissecting microscopy and histological appearance of the biopsies were normal (Gd 0-1) except for two which showed grade 2 changes. tbiopsy morphometry showed a reduction of jejunal mucosal surface area and an increase in mucosal volume in patients with Chron's disease when compared with the other two groups. The mucosal enzymes studies demonstrated that patients with Crohn's disease had a significant reduction in brush-border enzymes (disaccharidase) but no change in cytoplasmic enzyme activity (dipeptidases). The enzyme levels in patients with ulcerative colitis did not differ from the healthy controls. The reduction of brush-border enzymes with normal cytoplasmic enzymes in the presence of abnormal morphometry is further evidence of the concept of Crohn's disease as a diffuse lesion of the gastrointestinal tract. It also suggests that there is either specific damage to the microvilli or some other abnormality such as impairment of enzyme synthesis.