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PubMed1998

Role of reactive oxygen species in Salmonella typhimurium-induced enterocyte damage.

BACKGROUND: Reactive oxygen species (ROS) are potent mediators of inflammatory cell-mediated tissue destruction and may be of pathophysiologic importance in Salmonella typhimurium-induced tissue damage. METHODS: In this study the ligated rat ileal loops were injected with Salmonella live culture or toxin. The ROS generation was detected by measuring the mucosal myeloperoxidase (MPO) activity; the enterocyte xanthine oxidase (XO) activity, and the chemiluminescence response of gut macrophages. The enterocyte damage was estimated by measuring the extent of lipid peroxidation and cell viability. RESULTS: Treatment with Salmonella live culture or toxin resulted in an increase in the mucosal MPO activity, the enterocyte XO activity, and the chemiluminescence response of macrophages. Treated loop enterocytes had an increased extent of lipid peroxidation and decreased cell viability. Cell viability was also decreased when the enterocytes were co-cultured with macrophages isolated from the treated loops. Lipid peroxidation decreased, and cell viability increased in the presence of superoxide dismutase (SOD) or catalase. CONCLUSIONS: The S. typhimurium-mediated intestinal infection is accompanied by an increased generation of ROS, which may induce the lipid peroxidation of the enterocyte membrane, thereby leading to a loss of cell viability.

Animals↗
PubMed1979

Element concentration changes in mitotically active and postmitotic enterocytes. An x-ray microanalysis study.

Unfixed freeze-dried and uncoated tissue sections of the mouse duodenum were suspended across a hole in a carbon planchet and analyzed in a scanning electron microscope fitted with energy-dispersive x-ray analytical equipment. Computer analysis of the x-ray spectra allowed elemental microanalysis of the nucleus, cytoplasm, and late anaphase-early telophase chromatin regions in the cryptal and villus enterocytes. Elemental concentrations (mmol/kg dry wt) were measured for Na, Mg, P, S, Cl, K, and Ca. None of the elements were compartmentalized preferentially in either the nucleus or the cytoplasm of interphase enterocytes of crypts or in postmitotic enterocytes of villi. In contrast, Ca, S, and Cl are detectable in significantly higher concentrations in mitotic chromatin of dividing enterocytes of the crypt as compared to surrounding mitotic cytoplasm, but Na, Mg, and P are in lower concentrations in the mitotic chromatin as compared to mitotic cytoplasm. Interphase enterocytes of crypts have higher concentrations of Mg, P, and K, and lower concentrations of Na than do postmitotic enterocytes of villi.

Animals↗
PubMed1990

Effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes.

In vitamin A-deficient children, increased rates of bacterial infections in the intestine have been observed. The adherence of bacteria is a prerequisite for invasion. Thus, the effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes was studied. Male weanling rats matched by weight were divided into three groups: one group was fed a vitamin A-free diet for 8-12 weeks; another was given the same diet supplemented with retinol acetate; a third group matched for age served as controls. The vitamin A-deficient group showed a significantly lower growth rate and lower serum retinol levels than either the retinol acetate-supplemented or control groups. In all the groups, S. typhimurium possessing mannose-sensitive fimbriae adhered to enterocytes in significantly larger numbers than the nonfimbriated strains. The number of fimbriated S. typhimurium bound to enterocytes from the proximal small intestine was significantly higher in the vitamin A-deficient rats than in the pair-fed vitamin A-supplemented group (19.3 +/- 14.9 versus 7.8 +/- 5.0; p less than 0.05) or the control group (19.3 +/- 14.9 versus 8.7 +/- 3.5, p = 0.01). The specific activities of the enterocytes lactase, sucrase, and maltase and the protein content in the vitamin A-deficient rats were similar to those in the controls. These results demonstrate that vitamin A deficiency in rats is associated with the increased ability of S. typhimurium to adhere to proximal small intestinal enterocytes. However, the possible changes in the membrane of the enterocyte do not include decreases in brush border disaccharidases or protein content.

Animals↗
PubMed1997

Cell surface phenotype and ultramicroscopic analysis of purified human enterocytes: a possible antigen-presenting cell in the intestine.

Epithelial cells of the intestine seem to act as antigen-presenting cells to surrounding lymphoid tissue and may be crucial to maintain the pool of peripheral T lymphocytes. The scope of this study was to carry out an immunophenotypic and ultramicroscopic analysis of purified human enterocytes to elucidate their role as antigen-presenting cells, in the immune responses in the gut-associated lymphoid tissue. A method has been developed to obtain purified and viable human enterocyte populations, later labeled with relevant monoclonal antibodies directed to leukocyte antigens and subjected to cytofluorometric analysis. Phenotypic analysis revealed the presence of markers common to "classical" antigen-presenting cells (CD14, CD35, CD39, CD43, CD63 and CD64), reinforcing the idea that enterocytes may act as such. Moreover, several integrins (CD11b, CD11c, CD18, CD41a, CD61 and CD29) were also found. CD25 (IL-2 receptor alpha chain) and CD28, characteristic of T cells, were detected on the surface of these cells; this latter finding rises the possibility that enterocytes could be activated by IL-2 and/or via CD28 through binding to its ligands CD80 or CD86. Finally, the presence of CD21, CD32, CD35 and CD64 that may bind immune complexes via Fc or C3, suggests their participation in the metabolism of immune complexes. Furthermore, the finding of a Birbeck's-like granule in the cytoplasm of the cells, shows that enterocytes contain an ultramicroscopic feature previously thought to be characteristic of Langerhans' cells, an antigen-presenting cell. The phenotype detected on the surface of enterocytes, along with their ultramicroscopic characteristics, suggests that they may play an important role in the immune responses elicited in the gut, presenting antigens to surrounding lymphoid cells, and establishing cognate interactions with them.

Antigen-Presenting Cells↗
PubMed1991

Developmental control over vitamin-D-induced calbindin gene expression during early differentiation of chicken jejunal enterocytes.

In situ hybridization and immunocytochemical techniques have been used to examine the distribution of vitamin-D-induced calbindin mRNA and calbindin protein in enterocytes lining the crypts and villi of chicken small intestine. Basal villus enterocytes contained approximately twice as much calbindin but over three times as much calbindin mRNA compared to values found in basal crypt and upper villus enterocytes, all values being measured 2 days after vitamin D injection into D-deficient chickens. Virtually no calbindin mRNA was detected in tissues taken from control D-deficient birds. Direct proportionality found between calbindin mRNA and calbindin content in enterocytes of basal crypt, mid and upper villus suggests pre-translational control over calbindin synthesis. The implications of possible inefficient translation of calbindin mRNA in basal villus enterocytes are discussed. Present methods of analysis provide a novel way to study mechanisms controlling gene expression throughout the whole process of enterocyte differentiation.

Animals↗
PubMed1993

Intestinal arginine metabolism during development. Evidence for de novo synthesis of L-arginine in newborn pig enterocytes.

The capacity for L-arginine metabolism was studied in villus enterocytes isolated from pigs at birth, after 2-8 days suckling and after weaning. Immediately after birth, enterocytes were able to convert 1 mM L-citrulline, 2 mM L-glutamine or 1 mM L-ornithine to L-arginine. In 2-8-day-old animals, the net production of L-arginine from L-citrulline (2.00 +/- 0.45 nmol x 10(6) cells-1 x 30 min-1), or from L-ornithine (0.29 +/- 0.06 nmol x 10(6) cells-1 x 30 min-1) was similar to the values obtained at birth. Furthermore, 40% of L-arginine synthetized de novo from L-citrulline were released into the incubation medium. In 2-8-day-old animals, the production of L-arginine from L-glutamine represented only 5% of the production at birth (the latter being 0.73 +/- 0.15 nmol x 10(6) cells-1 x 30 min-1). In enterocytes isolated from post-weaned pigs, no significant production of L-arginine from either L-glutamine or L-ornithine was detected. In contrast, although the L-arginine production from L-citrulline was very low in post-weaned animals, it was significantly enhanced in the presence of L-glutamine, representing 23% of the production measured in suckling animals. The capacity of enterocytes to cleave L-arginine to L-ornithine and urea was very limited at birth, but was increased more than threefold in 2-day-old animals. This was concomitant with a marked increase in arginase activity. In post-weaned animals, the flux through arginase in intact enterocytes, and the arginase activity were both threefold higher than in 2-8-day-old animals. It is concluded that enterocytes isolated from neonatal pigs exhibit the capacity for a net production of L-arginine since the metabolism of this amino acid is oriented to anabolism rather than catabolism. The results are discussed in relation to L-arginine metabolism in the neonatal liver.

Animals↗
PubMed1994

The role of cyclic AMP in the control of sugar transport across the brush-border and basolateral membranes of rat jejunal enterocytes.

Although the involvement of the adenylate cyclase system with glucose transport in the small intestine is poorly understood, there is increasing evidence that cyclic AMP stimulates sugar uptake. In order to study further the effects of cyclic AMP on this process, we have measured glucose accumulation by brush-border and basolateral membrane vesicles prepared from villus enterocytes following exposure of these cells to cyclic AMP and theophylline. Brush-border vesicles derived from enterocytes incubated with cyclic AMP and theophylline accumulated significantly more glucose over a wide range of sugar concentrations, suggesting a change in maximum velocity of the transport system. Glucose uptake by basolateral vesicles was increased at low, but not at high sugar concentrations. Incubation of isolated enterocytes with pancreatic glucagon at concentrations known to stimulate sugar transport by these cells significantly increased enterocyte levels of cyclic AMP. Treatment with glucagon or cyclic AMP resulted in significant hyperpolarization of the potential difference across the brush-border membrane, an important driving force for Na(+)-sugar cotransport. The response to glucagon and cyclic AMP appears to be caused by a decrease in Na+ permeability of the mucosal membrane. Taken together, these results suggest that cyclic AMP is a mediator of the actions of glucagon on enterocytes and provide further evidence for a role of cyclic AMP in the modulation of sugar transport across the intestinal enterocyte.

Animals↗
PubMed1983

Effect of diet upon enterocyte differentiation in the rat jejunum.

Positional and temporal correlates for the development of microvillus membranes and for two of the hydrolytic enzymes they contain have been determined and compared with the ability of enterocytes to transport valine during migration from crypt base to villus tip in jejunal tissue taken from rats maintained on diets containing different amounts of protein. Microvillus elongation and the appearance of both aminopeptidase N (APN) and isomaltase (IM) activities reached maximal rates of expression in enterocytes located 16 +/- 5 micron from the crypt-villus junction. This close positional correlation was not found for the later development of the valine transport function. Feeding rats isoenergetic diets containing 20% instead of 5% protein caused significant increases in both villus height and crypt depth without changing the positional correlations described above. The maximal rates for microvillus elongation and APN and IM appearance were greater and occurred earlier in enterocytes taken from rats fed a high-protein diet. The time of onset and capacity to transport valine were found to be closely correlated for rats maintained on high- and low-protein diets. The ratio of APN to IM activity in fully differentiated enterocytes was either 0.7 or 1.2 depending on whether rats had been fed a low- or high-protein diet. The maximal length of microvillus membranes in fully differentiated enterocytes from rats on a low-protein diet was 1.4 times that found in rats maintained on a high-protein diet. Possible ways in which the microvillus membrane structure of enterocytes, enzyme activity and the ability to transport amino acids might be controlled are discussed. Relative estimates are also made of the probable effects that changes in diet will have on the capacity of the intestine to digest and absorb nutrients.

Aminopeptidases↗
PubMed1996

Role of calbindin-D9k in buffering cytosolic free Ca2+ ions in pig duodenal enterocytes.

1. The aim of the present study was to test whether the vitamin D-dependent Ca(2+)-binding protein calbindin-D9k could function as an important cytosolic Ca2+ buffer in duodenal enterocytes while facilitating transepithelial active transport of Ca2+ ions. For the investigations we used dual-wavelength, fluorescence ratio imaging, with fura-2 as the Ca(2+)-sensitive dye, to measure changes in cytosolic concentrations of free Ca2+ ions ([Ca2+]i) in isolated pig duodenal enterocytes affected by different cytosolic calbindin-D9k concentrations. 2. Epithelial cells were obtained from weaned piglets with normal calbindin-D9k concentrations (con-piglets), from piglets with low calbindin-D9k levels due to inherited calcitriol deficiency caused by defective renal 25-hydroxycholecalciferol D3-1 alpha-hydroxylase activity (def-piglets), and from piglets with reconstituted calbindin-D9k concentrations, i.e. def-animals treated with high doses of vitamin D3 which elevated plasma calcitriol levels by extrarenal production (def-D3-piglets). Basal levels of [Ca2+]i ranged between 170 and 205 nM and did not differ significantly between the groups. 3. After addition of 5 mM theophylline, the [Ca2+]i in enterocytes from con-piglets doubled during the 10 min incubation. This effect, however, was three times higher in enterocytes from def-piglets compared with those from con-piglets. Similar results were obtained after 4 min incubation of enterocytes from con- and def-piglets in the presence of 1 microM ionomycin. In preparations from def-D3-piglets, ionomycin-induced increases in [Ca2+]i were significantly lower compared with enterocytes from def-piglets and were not different from the control values. 4. From the results, substantial support is given for the hypothesis that one of the major functions of mucosal calbindin-D9k is the effective buffering of Ca2+ ions.

Animals↗
PubMed1985

Development of resistance of enterocytes to rotavirus in neonatal, agammaglobulinemic piglets.

The first part of this report describes the development of a technique for evaluating the growth of rotavirus under controlled conditions that approximate a natural infection. A standard dose of rotavirus (approximately 10(9) viral particles) was injected into ligated segments in the small intestine of newborn, agammaglobulinemic, colostrum-deprived piglets. After various periods postinoculation, the segments were retrieved and the enterocytes were evaluated for the presence of rotaviral antigens by immunofluorescence and rotaviral particles by transmission electron microscopy. Peak immunofluorescence in enterocytes was detected at 8 h postinoculation in the upper and middle jejunum and ileum. Transmission electron microscopy at this time revealed fully formed virions which were not seen in sections examined before this 8-h period. The second part of our study describes the use of ligated segments in determining the susceptibility to rotavirus of enterocytes in piglets ranging in age from newborn to 2 weeks. By the time piglets were 2 days old, enterocytes in the upper half of the small intestines appeared to be resistant to rotavirus, whereas those in the lower half seemed partially resistant. Between 4 and 8 days of age, enterocytes in the lower half also became resistant. Resistance paralleled the loss in capacity of piglets to transport macromolecules through enterocytes and was not correlated with the loss in capacity to internalize macromolecules.

Agammaglobulinemia↗
PubMed1990

Effect of vasoactive intestinal peptide on cyclic adenosine monophosphate production in enterocytes isolated from human duodenal biopsy specimens.

A modification of a cell isolation technique used in animal studies was developed to remove enterocytes from duodenal biopsy specimens. Citrate-ethylenediaminetetra-acetic acid treatment removed enterocytes from any underlying lamina propria and produced single cells and strips of cells. A mean (SEM) of 4.39 (2.06) x 10(6) cells was obtained from nine duodenal biopsy specimens. Enterocyte recovery was estimated enzymatically using alkaline phosphatase activity and was found to be 61%. Cytological assessment of the cells with CAM 5.2 showed that 98% of the cells isolated were enterocytes with an intact brush border. The cells responded well to vasoactive intestinal peptide stimulation in the absence of an exogenously added adenosine triphosphate regenerating system. The addition of vasoactive intestinal peptide to duodenal enterocytes produced a biphasic dose dependent increase in cyclic adenosine monophosphate production. Stimulation of these cells with 10(-13)M vasoactive intestinal peptide resulted in a 50% stimulation over basal value while 10(-6)M vasoactive intestinal peptide led to a fivefold increase in cyclic adenosine monophosphate production. We conclude that duodenal biopsy specimens are a good source of human intestinal cells for the study of enterocyte physiology. The cells were viable and highly responsive to vasoactive intestinal peptide.

Adult↗
PubMed1999

Identification of common epitopes on gliadin, enterocytes, and calreticulin recognised by antigliadin antibodies of patients with coeliac disease.

BACKGROUND: Sera of patients with coeliac disease, containing IgA and IgG antigliadin antibodies (AGA) and various IgA autoantibodies, react with isolated enterocytes. AGA cross react with enterocyte antigens, one of which has been identified as calreticulin. AIMS: To characterise the antigenic structures of gliadin, enterocytes, and calreticulin recognised by AGA from patients with active coeliac disease. METHODS: AGA were isolated from sera of nine patients by affinity chromatography and tested by competitive ELISA using 40 alpha-gliadin synthetic dodecapeptides (A1-F6). RESULTS: Reactivity of gliadin with all purified AGA tested was inhibited by peptide A4 at the N-terminal region; by C2, C3, and D4 at the central region; and by F3 and F4 at the C-terminal region of the gliadin molecule. AGA cross reactivity with enterocytes was inhibited by peptides A4, D1-D4, and F6 and with calreticulin by peptides A4, D3, and D4. As dominant epitopes AGA of coeliac patients recognise similar structures corresponding to peptides A4, D3, D4, and F6 present on gliadin, enterocytes, and calreticulin. Substitution of glutamine in the A4 peptide by glutamic acid caused loss of inhibitory capacity. Shortening of peptide A4 on the N-terminal by three amino acids increased its inhibitory effect. CONCLUSIONS: AGA of patients with coeliac disease react with similar structures on gliadin and potential autoantigens on enterocytes.

Adult↗
PubMed1986

Effect of refeeding on polyamine biosynthesis in isolated enterocytes.

Ornithine decarboxylase (ODC) activity has been found to be preferentially associated with small intestinal villus cells rather than crypt cells in the rat. In the present study, ODC, S-adenosylmethionine decarboxylase (SAMDC), and polyamines were measured in isolated enterocytes to determine which cell populations increased polyamine biosynthetic activity after refeeding. Two hours following refeeding, significant increases in ODC were observed in villus tip (10 times) and midvillus (20 times) enterocytes. No increase in ODC activity was found in isolated crypt cells. A similar pattern was observed for SAMDC. Enzyme activity increased in villus tip (2 times) and midvillus (27 times) cells but not in crypt enterocytes. Putrescine contents were increased following refeeding in midvillus enterocytes (P less than 0.05) and in crypt cells (P less than 0.05). The accumulation of putrescine in midvillus cells occurs via ODC-induced biosynthesis, whereas in crypt enterocytes it may be due to putrescine uptake. The lack of induction of ODC and SAMDC in crypt enterocytes following acute refeeding suggests these enzymes are apparently not involved in the initiation of cell proliferation known to occur under this condition.

Adenosylmethionine Decarboxylase↗
PubMed1986

Formation and transport of chylomicrons by enterocytes to the lymphatics.

Digestion of triglyceride in the intestine results in the production of 2-monoglyceride and fatty acid. Phosphatidylcholine is hydrolyzed in the lumen to form lysophosphatidylcholine before its absorption. These digestion products are absorbed by the enterocytes through simple diffusion. In contrast, cholesterol absorption seems specific and is energy dependent. After entry into the enterocytes, these lipid digestion products migrate to the endoplasmic reticulum. Both fatty acid-binding protein and sterol carrier protein may be involved in the intracellular transport of fatty acid and cholesterol, respectively. Through predominantly the monoglyceride pathway, monoglycerides and fatty acids are resynthesized to form triglyceride in the endoplasmic reticulum. The lipid droplets, coated with cholesterol, phospholipid, and apolipoproteins, are then further processed in the Golgi apparatus before being released by the enterocytes through exocytosis. As yet, little is known of the factors regulating the formation and release of these chylomicrons by the enterocytes. Although apolipoprotein B is a prerequisite for the formation of chylomicrons, the question of whether its supply is rate limiting for chylomicron formation remains to be demonstrated. Other factors that may play a role in chylomicron formation are luminal phospholipid supply, Ca2+, and microtubules. Chylomicrons and very low-density lipoproteins are probably produced by the enterocytes via different pathways. For example, Pluronic L-81, a hydrophobic surfactant, affects only chylomicron formation and has little effect on very low-density lipoprotein production. The movement of chylomicrons from the intercellular space through the basement membrane to the lamina propria is not fully understood. Once inside the lamina propria, the movement of chylomicrons is probably by diffusion and is greatly facilitated by interstitial hydration; thus the lymphogogic effect of fat absorption may serve an important function for the transfer of chylomicrons from the enterocytes to the lacteal.

Animals↗
PubMed1996

Chylomicron remnant uptake by enterocytes is receptor dependent.

During glyceryl trioleate absorption in the rat, mucosal triacylglycerol (TG) fatty acids have been shown to consist of only 71% exogenous oleate. Chylomicron remnants are enriched with endogenous TG fatty acids, compared with their parent chylomicrons, which consist primarily of exogenous TG fatty acids. Because enterocytes have the apolipoprotein B-100/E receptor, this study was directed at determining whether the cells can take up and metabolize chylomicron remnants and, if so, whether this was receptor mediated. Isolated enterocytes were incubated with purified 3H-labeled chylomicron remnants. The remnants were shown to be taken up by the basolateral membrane, not the apical membrane. Remnant uptake was proportional to time and number of enterocytes, and saturation kinetics were observed. Nonradiolabeled remnants, human low-density lipoprotein (LDL), anti-LDL receptor antibody, and receptor-associated protein, an LDL-related receptor inhibitor, were all shown to compete for or reduce 3H-remnant uptake. Remnants taken up by the enterocytes could not be removed on incubation with excess human LDL. Uptake was shown to be greatest in the villus tips of the proximal intestine. These studies suggest that enterocytes take up chylomicron remnants by a receptor-mediated process from their basolateral membranes and that the remnants could provide a source of endogenous TG fatty acids for the enterocytes.

Alkaline Phosphatase↗
PubMed1995

Arginine synthesis in enterocytes of neonatal pigs.

Arginine is deficient in porcine colostrum and milk, and yet the piglet has a particularly high requirement for this essential amino acid for rapid postnatal growth. To explain this paradox, arginine synthesis was quantified in enterocytes from newborn (0-day-old) and 2- to 7-day-old suckling pigs. Arginine was found to be synthesized from glutamine in 0- to 7-day-old pig enterocytes, but the rates of arginine synthesis were three- to fourfold greater in 0- to 2-day-old pigs than in 7-day-old pigs. To elucidate the developmental change of the intestinal arginine synthesis, the metabolism of glutamine to citrulline, the conversion of citrulline to arginine, and the activities of the enzymes involved were measured. The rates of metabolism of glutamine to citrulline were 2.5- to 3.5-fold greater in enterocytes from 0- to 2-day-old pigs than in cells from 7-day-old pigs, as were the rates of conversion of citrulline to arginine. The activities of all enzymes that synthesize arginine from glutamine, except pyrroline-5-carboxylate synthase and argininosuccinate lyase (ASL), increased in enterocytes from 2-day-old pigs compared with 0-day-old pigs. The activities of all these enzymes decreased by approximately 75% in 7-day-old pigs compared with 2-day-old pigs. Arginase activity was negligible in enterocytes from 0- to 7-day-old pigs, thus minimizing intestinal hydrolysis of newly synthesized arginine and maximizing the endogenous provision of arginine. The results of this study demonstrate the presence of arginine-synthesizing enzymes and their developmental changes in postnatal pig enterocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1994

Small intestine hexose transport in experimental diabetes. Increased transporter mRNA and protein expression in enterocytes.

The effect of insulinopenic diabetes on the expression of glucose transporters in the small intestine was investigated. Enterocytes were sequentially isolated from jejunum and ileum of normal fed rats, streptozotocin-diabetic rats, and diabetic rats treated with insulin. Facilitative glucose transporter (GLUT) 2, GLUT5, and sodium-dependent glucose transporter 1 protein content was increased from 1.5- to 6-fold in enterocytes isolated from diabetic animals in both jejunum and ileum. Insulin was able to reverse the increase in transporter protein expression seen after induction of diabetes. There was a four- to eightfold increase in the amount of enterocyte glucose transporter mRNA after diabetes with greater changes in sodium-dependent glucose transporter 1 and GLUT2 than in GLUT5 levels. In situ hybridization showed that after the induction of diabetes there was new hybridization in lower villus and crypt enterocytes that was reversed by insulin treatment. Thus, the increase in total hexose transport caused by diabetes is due to a premature expression of hexose transporters by enterocytes along the crypt-villus axis, causing a cumulative increase in enterocyte transporter protein during maturation. These changes are likely to represent an adaptive response by the organism to increase nutrient absorption in a perceived state of tissue starvation. These adaptive changes may lead to exacerbation of hyperglycemia in uncontrolled diabetes.

Amino Acid Sequence↗
PubMedDate not supplied

Effect of an elemental vs a complex diet on polyamine metabolism in rat isolated enterocytes.

BACKGROUND: Polyamines play an important role in the proliferation and differentiation of enterocytes. Ornithine decarboxylase (ODC) is the rate-limiting enzyme for polyamine biosynthesis. Elemental diets, providing easily absorbable nutrients such as free amino acids, are used in clinical practice to treat growth failure and malnutrition. They are very different from complex diets normally consumed. Little information is available about the influence of elemental diets on metabolic capacities of enterocytes. This study was undertaken in rats to assess the effects on polyamine metabolism of an elemental diet compared with a complex diet. METHODS: Rats were fed the elemental diet (group ED) or the control diet (group C) for 14 days. The dietary intakes were isocaloric and isonitrogenous in groups C and ED. Villous enterocytes were then isolated and metabolic capacities or enzyme activities were assessed. RESULTS: Both the enterocyte capacity to decarboxylate ornithine through ODC (measured in viable enterocytes) and ODC activity (measured in homogenates) were severely decreased in group ED. The polyamine content in enterocytes, however, was maintained at a similar level in both groups. This coincided with a decrease in the main enzymatic activity responsible for putrescine catabolism (ie, diamine oxidase activity) in group ED. CONCLUSIONS: Although nutrition manipulation was shown to alter polyamine biosynthesis in this study, the polyamine homeostasis was probably maintained, at least in part, through down-regulation of diamine oxidase.

Amine Oxidase (Copper-Containing)↗