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PubMed1989

Evidence for critical-period programming of intestinal transport function: variations in the dietary ratio of polyunsaturated to saturated fatty acids alters ontogeny of the rat intestine.

2-week isocaloric modifications in the dietary ratio of polyunsaturated/saturated fatty acids (P/S) alters intestinal transport in rats. This study was undertaken to test the hypotheses that (1) the fatty acid composition of a nutritionally adequate diet in early life has lasting consequences for active and passive intestinal transport processes; and (2) early life feeding experiences with diets of varying fatty acid composition influence the intestines' ability to adaptively up- or down-regulate intestinal transport in later life. Female Sprague-Dawley rats were weaned onto S or P and were maintained on these diets for 2, 10 or 12 weeks. An in vitro uptake technique was used in which the bulk phase was vigorously stirred to reduce the effective resistance of the intestinal unstirred water layer. P decreased and S increased the uptake of glucose, and this effect was progressive from 2 to 12 weeks. Switching from a P to an S diet decreased jejunal but increased ileal uptake of glucose, whereas switching from an S to a P diet was associated with a decline in both the jejunal and the ileal uptake of glucose. The ileal uptake of galactose increased as the animals grew on either P or S. Switching from P to S resulted in a decline in ileal uptake of galactose, whereas the opposite effect was observed when switching from S to P. The effect of feeding P or S on hexose uptake was influenced by the animals' dietary history: ileal glucose and galactose uptake was lower in animals fed P at an early age (PSP) than in animals fed P for the first time in later life (SSP). Jejunal glucose and galactose uptake was also lower in animals fed S at an early age (SPS) than in those fed S for the first time in later life (PPS). The alterations in the uptake of long-chain saturated and unsaturated fatty acids and cholesterol did not progress with longer periods of feeding, and in the jejunum, lipid uptake did not change when switching from P to S or S to P. Early feeding with P (PSP vs. SSP) was associated with lower jejunal uptake of 18:3 and lower ileal uptake of 12:0, whereas previous feeding with S (SPS vs. PPS) was associated with lower ileal uptake of cholesterol. The changes in uptake of hexoses and lipids was not explained by differences in the animals' food consumption, body or intestinal weight or mucosal surface area.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Light and electron microscopic immunocytochemical localization of vasoactive intestinal polypeptide VIP-like activity in the rat small intestine.

Vasoactive intestinal polypeptide nerve processes and cell bodies were identified by electron microscopic immunocytochemistry in the rat small intestine. Labeled nerve processes were numerous in the inner circular smooth muscle coat and mainly in the mucosa, but were absent in the longitudinal muscle layer. Submucosal blood vessels were often surrounded by immunoreactive vasoactive intestinal polypeptide positive nerves, in close associations (distance less than 40 mn) to blood vessel basement membranes and to smooth muscle cells. In the ganglia of the myenteric and submucous plexuses, labeled fibers surrounded unstained neural cell bodies. The synaptic vesicles of vasoactive intestinal polypeptide positive terminals were 35-40 nm in diameter and some dense core vesicles (80-120 nm in diameter) were also observed in the same profiles. These observations suggest that vasoactive intestinal polypeptide nerves may participate in regulating smooth muscle activity and local blood flow in the small intestine.

Animals↗
PubMed1994

Reappraisal of the innervation of rat intestine by vasoactive intestinal polypeptide and neuropeptide Y-immunoreactive neurons.

The occurrence and distribution of neurons and nerve fibres showing vasoactive intestinal polypeptide-like and neuropeptide Y-like immunoreactivity were re-examined in the enteric nervous system of the small and large intestine of the adult rat using dual-labelling indirect immunofluorescence histochemistry to detect the co-existence of these neuropeptides. In the myenteric plexus of both small and large intestine, a population of neuropeptide Y-immunoreactive neurons that did not contain vasoactive intestinal polypeptide was noted; it accounted for 29-53% of neuropeptide Y neurons. Such neurons were also found in the submucosa but there they constituted at most 2% of neuropeptide Y-immunoreactive neurons. In both myenteric and submucous plexuses, regional variations were observed in the number of immunoreactive neurons and in the proportion of dual-labelled neurons. In the myenteric plexus, for example, the density of neurons with immunoreactivity to these two neuropeptides was constant throughout the small intestine, whereas it progressively increased distally within the colon. In addition, a distinct but small subset of immunoreactive myenteric neurons was found to have a novel soma morphology, unclassifiable according to the criteria used for porcine or guinea-pig enteric neurons. Such neurons had one or more conspicuous processes, which were much longer than the short, lamellar somal processes of typical Dogiel Type 1 neurons; moreover, these protruded from an essentially smooth soma and terminated at distances of up to two cell diameters from their point of origin. Thus, our results suggest that the organization of the enteric nervous system of the rat differs from that of other species and indicate that investigation of the co-localizations of neuropeptides and biologically active mediators in the intestinal tract would be incomplete without reference to regional differences in the incidence and distribution of such neurochemicals.

Animals↗
PubMed1987

Hypertonicity of intestinal smooth muscle as a factor of intestinal ischemia in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is thought to be secondary to mucosal ischemia. Because blood flow to the submucosal plexus is derived from vessels traversing three separate layers of visceral smooth muscle (longitudinal, circular, and muscularis mucosa), we investigated whether an increase in their tone might elicit mucosal ischemia. The intestinal intraluminal pressure (IIP) and the superior mesenteric artery (SMA) blood flow were evaluated in 23 dogs before and after either ligation of the SMA or neostigmine infusion into the SMA. Changes in vascularity were assessed by silicone rubber casting, India ink, or arteriography. Ten minutes after ligation of the SMA, there was a considerable increase in peristalsis, IIP, and inability to fill the intestinal microcirculation by the three methods described. Mucosal necrosis was present three hours later. In the neostigmine infusion group after a transient increase in mesenteric flow, the IIP rose 750%, while the mesenteric flow fell by 40%, mucosal necrosis occurred in one hour. When myotomy was performed on the antimesenteric border, mucosal necrosis was prevented. In a third group, neostigmine infused (femoral artery) in the hind limb demonstrated vasodilating effects. The data indicate that an increase in the myogenic tone and frequency of contraction of intestinal smooth muscle can produce mucosal ischemia, thus, intestinal hypertonicity may be an important factor in the pathogenesis of intestinal ischemia and possibly NEC. The effects of neostigmine in these experiments raise questions regarding its use during anesthesia in neonates with intestinal low flow states.

Animals↗
PubMed1999

Factors impacting the survival of children with intestinal failure referred for intestinal transplantation.

PURPOSE: The aim of this study was to analyze factors impacting on the survival of pediatric patients with intestinal failure referred for intestinal transplantation (ITx). METHODS: Two hundred fifty-seven children (mean age, 3.4+/-0.26 years) with intestinal failure were evaluated for ITx between 1990 and 1998. All patients were dependent on total parenteral nutrition (TPN) for a mean of 31+/-2.7 months. The mean follow-up time from the date of evaluation was 9.2+/-0.9 months. RESULTS: Eighty-two (32%) children underwent ITx with a mean waiting time of 10.1+/-1.3 months (simultaneous liver-intestinal allograft in 68% instances). Of the 175 patients who did not undergo transplantation, 120 died, 23 were lost to follow-up, and 32 are alive. Younger patients (< or =1 year) had poorer survival rates than patients older than 1 year (P<.0001). The patients with the worse prognosis were those with necrotizing enterocolitis, and those with the best prognosis were those with Hirschsprung's disease. Patients with "surgical" causes had poorer survival rates than those with "nonsurgical" causes (P<.04). Patients with bridging fibrosis or established cirrhosis had an earlier mortality than patients with portal fibrosis (P<.003). The worst survival rate was found for patients with bilirubin levels of greater than 3 mg/dL (P<.0001), plateletcounts less than 100.000/mL (P<.0001), prothrombin time greater than 15 seconds (P = .03) or partial thromboplastin time greater than 40 seconds (P<.04). Children who at the time of evaluation needed only an isolated intestinal allograft had a better prognosis than those who required a combined liver-intestine allograft (P<.00001). With multivariate analysis independent prognosis risk factors of poor outcome were hyperbilirubinemia and severity of histopathologic damage. CONCLUSIONS: Early referral for ITx should occur before the development of liver dysfunction, taking into consideration the aforementioned risk factors that would facilitate the development and ominous evolution to liver failure.

Child, Preschool↗
PubMed1996

Current results of intestinal transplantation. The International Intestinal Transplant Registry.

BACKGROUND: Intestinal transplantation is an alternative to total parenteral nutrition (TPN) for the treatment of chronic intestinal failure. To determine the current status of small-bowel transplantation, we have reviewed the world experience since 1985. METHODS: We built up an international registry by asking twenty-five intestinal transplantation programmes to submit standard data on their cases operated on between 1985 and June, 1995. FINDINGS: One centre (two transplantations) did not use our report form, and these cases were excluded. The remaining twenty-four programmes did 180 transplantations in 170 patients. Two-thirds of the recipients were children. The main indication (64 percent) was short-gut syndrome, another 13 percent had a tumour. Of the grafts, 38 percent were small-bowel with or without colon, 46 percent were intestine plus liver, and 16 percent were multivisceral. Graft/patients' survival (percent) at 1 and 3 years under cyclosporin immunosuppression was, respectively: 17/57 and 11/50 for small bowel only; 44/44 and 28/28 for intestine plus liver; and 41/41 and 41/41 for multiviscera. The corresponding figures under tacrolimus were: 65/83 and 29/47; 64/66 and 38/40; and 51/59 and 37/43. 78 percent of the 86 survivors had stopped TPN and resumed oral nutrition. INTERPRETATION: Our approach cannot give data on long-term outcome. The short-term results of intestinal transplantation are similar to those of lung grafting. We conclude that small-bowel transplantation has become a life-saving option for patients who cannot be maintained on TPN and for those who require massive abdominal evisceration for locally aggressive tumours.

Adolescent↗
PubMed2002

Immunolocalization of a new intestinal antiproliferative factor in human intestinal epithelial cells.

A new intestinal antiproliferative factor (IAF) with an approximate molecular weight of 120 kDa has been purified from the human small intestine. This factor blocks the progression of human colon adenocarcinoma cells HT-29 from the G1 to the S phase. IAF, specific of the lower part of the digestive tract, was detected rather late in mouse embryonic development. For determination of the specific intestinal cell producing IAF, long-term differentiated mucus-secreting HT-29 Cl 16E and enterocytic HT-29 Cl 19A cell lines were used. IAF is synthesized exclusively in the intestinal goblet cells; it is processed in the RER and Golgi complex before being excreted in secretory vesicles independently of mucin secretion. IAF can be considered a growth inhibitor of intestinal proliferation for the same reason as TGF-beta. However, two features differentiate it from TGF-beta: (1) the intestinal cell type synthesizing it, and (2) the delay in its expression in embryonic development. Particular interest was paid to IAF expression in pathological conditions using human colon biopsies. IAF was consistently recovered in biopsies from patients with inflammatory bowel diseases and benign tumors, but it was never detected in malignant tumors. IAF could represent a marker of colon cancer owing to its absence from malignant tumors.

Adenocarcinoma↗
PubMed1997

Exocytotic release of vasoative intestinal polypeptide and serotonin from mucosal nerve fibres and endocrine cells of the intestine of the goldfish (Carassius auratus) and the tilapia (Oreochromis mossambicus): an ultrastructural study.

In earlier studies were determined the effect, presence and ultrastructure of vasoactive intestinal polypeptide (VIP) and 5-hydroxytryptamine (5-HT)-containing nerve fibres in the tilapia and goldfish intestinal mucosa. 5-HT-labelled varicosities were found close to the epithelial cells; however, synaptic membrane specializations have never been observed. VIP-like immunoreactive nerve fibres appear to be located less frequently close to the goldfish epithelium, as in the tilapia intestine, in which the distance between the VIP- or 5-HT-labelled varicosities and the epithelial cells was also rather large (more than 2 micros). To establish a possible role of VIP and 5-HT as neurotransmitters involved in the regulation of fish intestinal epithelium both electron microscopical and immunoelectron microscopical methods were used to visualize the release of 5-HT and VIP from nerve fibres. We found exocytoses from VIP-ergic and serotonergic varicosities in the muscle layers of both fish. Directly underneath the intestinal epithelium of the goldfish, it was demonstrated that 5-HT could be released from scarce varicosities. The release of 5-HT in the tilapia intestinal mucosa could only be observed from endocrine cells.

APUD Cells↗
PubMed2003

Effect of epidermal growth factor administration on intestinal cell proliferation, crypt fission and polyp formation in multiple intestinal neoplasia (Min) mice.

Recombinant epidermal growth factor (EGF) may be useful to treat severe ulcerative gastrointestinal injury. There is concern, however, that systemic use of this potent mitogen might increase tumour development and/or progression in susceptible subjects. We therefore examined the effect of chronic administration of systemic EGF to multiple intestinal neoplasia (Min ) mice, who have a genetic defect in the adenomatous polyposis coli (APC) gene, leading to increased polyp development. Min mice (n =26) and wild-type littermates (n =26) received saline or EGF (223 microg of EGF/kg per day) for 4 weeks using subcutaneous osmotic mini-pumps. Cell proliferation and crypt fission were analysed using microdissection techniques and the number and size of polyps in the small and large intestines were determined. EGF increased wet weight and crypt cell proliferation rate by approx. 20% (all P <0.01 compared with the relevant control) in the small intestine and colon of both control and Min mice. In both groups, EGF reduced the colonic fission index by approx. 40% (P <0.01), but did not affect crypt fission in the small intestine. In Min mice, administration of EGF did not increase numbers of polyps or degree of dysplasia, but resulted in a 40% increase in the polyp size in the proximal intestine (P <0.02), but not in the remainder of the small intestine or colon. No polyps were found in control mice given EGF. EGF did not initiate polyp formation in control or Min mice. However, as polyp size is an important determinant for subsequent risk of malignant change in human colon cancer, further studies appear justified.

Adenomatous Polyposis Coli↗
PubMed2002

Intestinal and renal handling of oxalate in magnesium-deficient rats. Evaluation of intestinal in vivo 14C-oxalate perfusion.

OBJECTIVE: To clarify in vivo, using isolated small intestinal loops perfused with radioactive 14C-oxalate, whether intestinal hyperabsorption or reduced secretion is important in magnesium deficiency (MgD), as this is a potential cause of calcium oxalate urolithiasis. MATERIALS AND METHODS: Twenty-four Sprague-Dawley rats were either fed a standard diet (control, 12 rats) or a magnesium-deficient diet (MgD, 12 rats) for 19 weeks. One hour before the animals were killed, a defined length of a small intestinal loop was isolated and filled with 5 mL of 0.9% NaCl and a defined amount of intravenous 14C-oxalate applied. Using this method it was possible to determine the secretion of unlabelled oxalate into the intestinal lumen, from the specific activity in plasma. RESULTS: Plasma oxalate levels doubled under MgD; urinary calcium and phosphorus also increased significantly, while urine oxalate tended to decrease. The secretion of oxalate into the intestinal lumen of MgD animals increased significantly, by five times that of the control. The relative supersaturation for calcium oxalate remained constant. Elementary analysis of renal tissue showed an increase in calcium and phosphorus under MgD, in the sense of nephrocalcinosis, but no concretions were detected (no nephrolithiasis). CONCLUSION: In contrast to earlier studies, there is no evidence that hyperoxaluria is responsible for the possible development of urolithiasis in MgD. This was confirmed by calcium phosphate deposits in renal tissue, even though there was no evidence of oxalate urolithiasis. The increase in plasma oxalate seems to be completely compensated by strongly increased oxalate secretion into the intestinal lumen.

Animals↗
PubMed2002

CDX2 regulates liver intestine-cadherin expression in normal and malignant colon epithelium and intestinal metaplasia.

BACKGROUND & AIMS: The intestine-specific caudal-related homeobox transcription factor CDX2 seems to play a key role in intestinal development and differentiation. Inactivation of one Cdx2 allele predisposes mice to develop colon polyps, and loss of CDX2 expression is a feature of some poorly differentiated colon carcinomas in humans. Conversely, aberrant CDX2 expression is often seen in intestinal metaplasias in the stomach and esophagus and in some gastric carcinomas. To better understand CDX2 function, we sought to define CDX2-regulated genes. METHODS: HT-29 colon cancer cells with minimal endogenous CDX2 expression were engineered to express exogenous CDX2, and gene expression changes relative to control cells were assessed using high-density oligonucleotide arrays. RESULTS: The gene for liver intestine (LI)-cadherin (cadherin 17) was strongly induced by CDX2 in HT-29. In other colorectal cancer lines, endogenous CDX2 and LI-cadherin expression were well correlated. Activation of a ligand-regulated form of CDX2 rapidly induced LI-cadherin gene expression, even in the presence of protein synthesis inhibitor. Analysis of the 5'-flanking region of the LI-cadherin gene defined 2 CDX2 responsive elements, and chromatin immunoprecipitation assays indicate CDX2 binds to the elements. In primary colorectal cancers and intestinal metaplasias in the stomach, CDX2 and LI-cadherin expression were tightly correlated. CONCLUSIONS: CDX2 regulates LI-cadherin gene expression in normal, metaplastic, and neoplastic tissues of the gastrointestinal tract via binding to elements in the 5'-flanking region of the gene. Given the well-established roles of cadherins in morphogenesis and differentiation, LI-cadherin may be a key factor mediating CDX2 function in intestinal cell fate determination.

Animals↗
PubMed2004

Intestinal transplantation for total/near-total aganglionosis and intestinal pseudo-obstruction.

Whether from anatomical short gut (such as after resection of extensive intestinal aganglionosis) or from a functional cause (such as intestinal pseudoobstruction), intestinal failure is a devastating disease process with profound morbidity and mortality. These patients require total parenteral nutrition (TPN) and are at risk of developing complications such as liver failure, catheter-related sepsis and loss of venous access. Intestinal transplantation, which has advanced markedly over the last 14 years, is now the accepted standard of care for patients failing TPN. Survival outcomes have improved significantly, infectious complications are better controlled, and new immunosuppressive therapies offer great hope for the future. In particular, the results of intestinal transplantation achieved with the motility disorders are equivalent to those experienced with other causes of intestinal failure. In themselves, the motility disorders present their own set of complicating factors, including determining the extent of the disease process (which may involve any part of the gastrointestinal tract), associated urological anomalies, and the type of organ transplantation required. Extensive workup and careful consideration is required before transplantation is undertaken. However, early referral is desirable once complications arise if these patients are to be offered optimal medical care before the chance of transplantation is lost.

Adult↗
PubMed2001

Body and intestinal growth of broiler chicks on a commercial starter diet. 2. Development and characteristics of intestinal enzymes.

1. Investigations were conducted into the development of intestinal enzyme function in broiler chickens on a commercial starter diet. The differences between intestinal regions and localisation of enzymes on the villus were assessed. 2. The specific activity of maltase, sucrase, aminopeptidase N (APN) and alkaline phosphatase (AP) at all intestinal sites decreased with age. There were also variations between intestinal sites although this variation depended on age. The specific activity of maltase was higher than that of the other enzymes examined, regardless of age and intestinal site. The total activities of the enzymes also increased with age at all intestinal sites. 3. Results of the localisation of enzymes on the crypt: villus axis showed that activity was expressed over a large proportion of the villus. There was an increase in the total villus activity of alpha-glucosidase (AG), APN and AP with age. Activity per unit villus surface area was similar between ages, except for jejunal AP. At hatch enzyme activity was expressed over 44.1, 55.8 and 63.3% of villus height in the duodenum, jejunum and ileum, respectively. At 21 d of age, corresponding values were 68.7, 65.6 and 77.2%. The point of peak activity from the crypt: villus junction increased with age. In the jejunum, most enterocytes were capable of secreting active enzymes within 1 h of formation. Cells maintained their secretory capabilities until they were more than 60 h old in the case of AG. 4. Although the specific activities of the enzymes were maximal at hatch, the digestive capacity of older birds may be sustained by an increase in total enzyme activity brought about by increased surface area. The pattern of enzyme activity along the gastrointestional tract (GIT) and crypt: villus axis is similar to that reported for some mammalian species.

Age Factors↗
PubMed2000

Active intestinal chloride secretion in human carriers of cystic fibrosis mutations: an evaluation of the hypothesis that heterozygotes have subnormal active intestinal chloride secretion.

To explain the very high frequency of cystic fibrosis (CF) mutations in most populations of European descent, it has been proposed that CF heterozygotes have a survival advantage when infected with Vibrio cholerae or Escherichia coli, the toxins of which induce diarrhea by stimulation of active intestinal chloride secretion. Two assumptions underlie this hypothesis: (1) chloride conductance by the CF transmembrane conductance regulator (CFTR) is the rate-limiting step for active intestinal chloride secretion at all levels of expression, from approximately zero in patients with CF to normal levels in people who are not carriers of a mutation; and (2) heterozygotes have smaller amounts of functional intestinal CFTR than do people who are not carriers, and heterozygotes therefore secrete less chloride when exposed to secretagogues. The authors used an intestinal perfusion technique to measure in vivo basal and prostaglandin-stimulated jejunal chloride secretion in normal subjects, CF heterozygotes, and patients with CF. Patients with CF had essentially no active chloride secretion in the basal state, and secretion was not stimulated by a prostaglandin analogue. However, CF heterozygotes secreted chloride at the same rate as did people without a CF mutation. If heterozygotes are assumed to have less-than-normal intestinal CFTR function, these results mean that CFTR expression is not rate limiting for active chloride secretion in heterozygotes. The results do not support the theory that the very high frequency of CF mutations is due to a survival advantage that is conferred on heterozygotes who contract diarrheal illnesses mediated by intestinal hypersecretion of chloride.

Adolescent↗
PubMed1994

Improving access to intestinal stem cells as a step toward intestinal gene transfer.

In previous studies exploring the intestinal epithelium as a potential site for somatic gene therapy, we concluded that the mucus lining the intestine constitutes a significant barrier to any attempts at gene transfer via the lumenal route. The mucus problem is aggravated by the fact that the epithelial stem cells, which are the logical target for gene transfer, are located deep in the intestinal crypts. The goals of the current study were to develop procedures that would improve accessibility to the intestinal stem cells and which would effect in vivo mucus removal without damaging the underlying epithelium. Initial experiments involved evaluation of the use of distension to improve accessibility to the intestinal crypts and the use of the mucolytic agents dithiothreitol (DTT) and N-acetyl-cysteine (NAC) versus a control solution of phosphate-buffered saline (PBS) for mucus removal. Catheters were inserted in each end of 3-cm terminal ileal segments in anesthetized rats. Two milliliters of agent was instilled into the clamped segment for 2 min, removed, and repeated. Lumenal distension resulted in shortened villi with wider intervillus spacing, thereby improving crypt access. Both NAC and DTT washes removed significant mucus between the villi but failed to reach the crypt lumen. To enhance mucus release from the crypt lumen, pilocarpine was selected due to its cholinergic properties and preferential binding to muscarinic receptors on crypt goblet cells. Pilocarpine given intraperitoneally 30 min prior to the mucolytic or PBS wash resulted in significant eradication of mucus down into the crypt lumen. This effect was still evident 3-4 hr later provided the intestine remained undisturbed.

Acetylcysteine↗
PubMed1982

FMN phosphatase and FAD pyrophosphatase in rat intestinal brush borders: role in intestinal absorption of dietary riboflavin.

Flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), are two major coenzyme forms of dietary riboflavin. Yet little attention has been given to the release of the vitamin from its coenzyme forms during the absorptive process. Homogenates from rat intestine catalyze the hydrolases of these flavin coenzymes. To determine the location of FMN and FAD hydrolases, homogenates of intestinal mucosa were fractioned. FMN and FAD phosphatases were localized in brush border membranes. FAD pyrophosphatase activity was maximal at pH between 6.5 and 8.5 while FMN phosphatase has a pH optimum of 7.5 - 8.0. FAD pyrophosphatase is more stable to heat. The two enzymes separate on ion exchange chromatography of an isobutanol extract of intestinal brush border membrane fraction. Inhibition of 14C-riboflavin uptake by FMN and FAd in everted rings of rat intestine is directly related to the amount of conversion of these coenzymes to free riboflavin by intestinal enzymes. When FMN and FAD conversion to riboflavin is inhibited by EDTA, competition with 14C-riboflavin for transport was correspondingly decreased. These studies are best explained by a sequential process in which hydrolysis of FMN and FAD by enzymes of the intestinal brush border is followed by absorption of free riboflavin.

Animals↗
PubMed1998

Weaning and the weanling diet influence the villous height and crypt depth in the small intestine of pigs and alter the concentrations of short-chain fatty acids in the large intestine and blood.

Effects of weaning pigs to different diets have been investigated in terms of the changes in the small intestinal morphology, and in the absorption of short-chain fatty acids (SCFA) and sodium from the large intestine. One piglet from each of six litters containing nine pigs was sampled on the day of weaning; the other eight piglets were divided into four equal groups and fed different diets as follows: unweaned, weanling diet, or sow's milk at high or low level. Four and seven days after weaning, measurements of the intestinal tissue and contents were made; the plasma concentrations of SCFA, aldosterone and sodium were also measured. The villous height in the small intestine was highest in the unweaned group and greater in the high milk group than in either the weanling diet or low milk group (P < 0.001). Apparently, villous atrophy was due more to the level of feed intake than to the composition of the diet. The concentrations of SCFA in the large intestine and portal blood were highest in the weanling diet group and lowest in the low milk group. The low milk group tended to have higher blood concentrations of aldosterone (P = 0.15), which may have compensated for the low concentrations of SCFA in maintaining a higher percentage of dry matter in the intestine. Pigs fed weanling diet may use the energy from the SCFA to maintain a body weight comparable to that of pigs fed milk at a low level.

Aldosterone↗
PubMed1999

Regenerative signals for intestinal epithelial organoid units transplanted on biodegradable polymer scaffolds for tissue engineering of small intestine.

BACKGROUND: Our laboratory is investigating the tissue engineering of small intestine using intestinal epithelial organoid units seeded onto highly porous biodegradable polymer tubes. This study investigated methods of stimulation for optimizing neointestinal regeneration. METHODS: Intestinal epithelial organoid units harvested from neonatal Lewis rats were seeded onto porous biodegradable polymer tubes and implanted into the omentum of adult Lewis rats in the following groups: (1) the control group (group C), implantation alone (n=9); (2) the small bowel resection (SBr) group, after 75% SBr (n=9); (3) the portacaval shunt (PCS) group, after PCS (n=8); and (4) the partial hepatectomy (PH) group, after 75% PH (n=8). Neointestinal cyst size was recorded using ultrasonography. Constructs were harvested at 10 weeks and were examined using histology. Morphometric analysis of the neomucosa was obtained using a computer image analysis program (NIH Image, version 1.59). RESULTS: Cyst development was noted in all animals. Cyst lengths and diameters were significantly larger in the SBr group at 7 and 10 weeks compared with the other three groups (P<0.05; analysis of variance [ANOVA], Fisher's protected least significant difference). Histology revealed a well-vascularized tissue with a neomucosa lining the lumen with invaginations resembling crypt-villus structures. Morphometric analysis demonstrated a significantly greater villus number, height, area, and mucosal surface in the SBr group compared with the other three groups and a significantly greater crypt number and area in the PCS group compared with group C (P<0.05; ANOVA, Fisher's protected least significant difference). CONCLUSIONS: Intestinal epithelial organoid units transplanted on porous biodegradable polymer tubes can successfully vascularize, survive, and regenerate into complex tissue resembling small intestine. SBr and, to a lesser extent, PCS provide significant regenerative stimuli for the morphogenesis and differentiation of tissue-engineered small intestine.

Animals↗