The present study was performed to examine the role played by pancreatotrophic factors, especially enteroglucagon and cholecystokinin (CCK), in the compensatory pancreatic hyperplasia observed after proximal small bowel resection (PSBR). Male Wistar rats were randomized into two groups, receiving either PSBR or transection (TRC). Five animals from each group were randomly selected for treatment with FK-480, a novel CCK antagonist. Four weeks after the operation, plasma levels of gastrin, CCK and enteroglucagon were measured. Pancreatic wet weight and protein, DNA, RNA and enzyme content were also determined. The wet weight and content of protein, DNA and RNA were significantly higher in PSBR rats than in TRC rats, regardless of whether they received FK-480. FK-480 had no suppressive effects on adaptive pancreatic growth after PSBR. Plasma enteroglucagon levels rose significantly in PSBR rats, and there were positive correlations between plasma enteroglucagon levels and pancreatic protein, DNA and RNA content. These findings demonstrated that plasma CCK was not the major trophic factor operating in the pancreas after PSBR, and showed that enteroglucagon plays an important role in the pancreatic hyperplasia that occurs after PSBR.

Animals↗

PubMedDate not supplied

Monitor peptide (rat pancreatic secretory trypsin inhibitor) directly stimulates the proliferation of the nontransformed intestinal epithelial cell line, IEC-6.

BACKGROUND/AIMS: The growth-stimulating activity of monitor peptide [rat pancreatic secretory trypsin inhibitor (PSTI)-61] was evaluated in the rat intestinal epithelial cell line IEC-6. In response to food intake, monitor peptide induces cholecystokinin release and the subsequent secretion of pancreatic enzyme into the rat small intestine. METHODS: Monitor peptide was purified from rat bile-pancreatic juice. The proliferation of IEC-6 cells was determined by both counting cell number and [3H]-thymidine incorporation. Ornithine decarboxylase (ODC) activity was assessed by radiometric technique using L-[1-14C]-ornithine. RESULTS: Monitor peptide (10(2)-10(5) ng/ml) induced a significant increase in the incorporation of [3H]-thymidine into IEC-6 cells, and this effect was observed in a dose-dependent manner. A significant increase in the cell number was also observed. An antibody specific for the synthetic NH2-terminal fragment of monitor peptide completely abrogated the growth-stimulating effects of this peptide. In addition, monitor peptide effectively increased the ODC activity of IEC-6 cells. CONCLUSIONS: These results indicate that monitor peptide stimulates the growth of intestinal epithelial cells, and suggest that polyamine metabolism may be involved in this mechanism of growth induction.

Animals↗

PubMedDate not supplied

Physiological and anti-inflammatory roles of dietary fiber and butyrate in intestinal functions.

BACKGROUND: We investigated the effects of pectin, a soluble dietary fiber, on the morphological parameters of the small intestine. In addition, we tested the effects of butyrate enemas on dextran sulfate sodium (DSS)-induced experimental colitis. METHODS: Male Wistar rats were fed an elemental diet containing 2.5% pectin for 14 days, and several parameters were then determined. DSS-induced colitis was evoked by the oral administration of water containing 3% DSS for 10 days. The butyrate enema (3 mL of 100 mmol/L butyrate per day) was begun 7 days before the DSS treatment. Interleukin (IL)-8 secretion in the human intestinal epithelial cell line HT-29 was determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Pectin feeding induced a significant increase in the villus height and crypt depth in the small intestine. These effects correlated with a significant increase in plasma enteroglucagon levels. Pretreatment with a butyrate enema significantly blocked the development of DSS-induced experimental colitis. In the in vitro experiment, sodium butyrate dose-dependently inhibited tumor necrosis factor (TNF)-alpha-induced IL-8 secretion in HT-29 cells. CONCLUSIONS: A trophic effect due to dietary fiber was directly observed. The generation of short-chain fatty acids and the induction of enteroglucagon release might play an important role in this process. Butyrate, one of the major metabolites of dietary fiber, exerted a potent anti-inflammatory effect both in vivo and in vitro. Dietary fiber may therefore play important roles in the regulation of normal and pathological conditions in the intestine.

Adenocarcinoma↗

PubMedDate not supplied

Polydextrose and activities of brush-border membrane enzymes of small intestine in rats and glucose absorption in humans.

We investigated the effect of polydextrose, one of the water-soluble non-digestible polysaccharides, on the activities of brush-border membrane enzymes of small intestine in rats and on glucose absorption with relation to the thickness of the unstirred water layer in humans. Rats were fed a 5% polydextrose-supplemented elemental diet for 2 or 4 wk. The mucosal alkaline phosphatase, maltase, and sucrase activities were measured in the upper, middle, and lower intestine. There was no significant difference between control and polydextrose groups. The potentiometric tube was inserted orally in the jejunum. Glucose absorption was measured by perfusion with the solutions with or without 5% polydextrose. There was no significant difference in the glucose absorption rate or the thickness of the unstirred water layer between control and polydextrose solutions. The increase in viscosity of the polydextrose solution was negligible. This study indicated that polydextrose had no effect on the thickness of the unstirred water layer and did not inhibit glucose absorption in humans.

Alkaline Phosphatase↗

PubMedDate not supplied

Effect of steam-heat treatment with/without divalent cations on the inactivation of lipopolysaccharides from several bacterial species.

The inactivation of endotoxin from six species of smooth gram-negative bacteria (S-form) by steam-heat treatment was investigated using the Limulus amebocyte lysate (LAL) assay. Biphasic decreases of endotoxins from four species of bacteria were observed upon steam-heat treatment of 1 microgram/ml endotoxin solution at 121 degrees C in a steam sterilizer. A lag time, however, was observed in the inactivation profiles of V. cholerae and P. aeruginosa. Distinct differences in heat resistance were observed among the bacterial species. The decrease rate was found to be concentration-dependent, and endotoxins at low concentrations (less than 10 ng/ml) were inactivated by the treatment to below the detection limit of the LAL assay. The time-course of the decrease of endotoxin from rough strains (R-form) resembled that of the respective S-form. The inactivation of R-form, especially Rc mutant, endotoxin was markedly affected by divalent cations such as Mg2+ and Ca2+, which appear to promote reaggregation of the endotoxin.

Calcium Chloride↗

PubMedDate not supplied

Enhancing effect of non-ionic surfactant on the inactivation of lipopolysaccharide by steam-heat treatment I.

Polyoxyethylene (20) sorbitan mono-fatty acid esters strongly enhanced the inactivation of lipopolysaccharide (LPS) by steam-heat treatment at 121 degrees C, as assayed by using the Limulus amebocyte lysate (LAL) and the pyrogen test. In an aqueous solution containing 0.1% surfactant, the decrease of LPS (1 microgram/ml) from E. coli 055:B5 at 121 degrees C followed first-order kinetics. Based on the LAL assay, 0.1% surfactant was essential to achieve 3-log cycle reduction of LPS with concomitant loss of pyrogenicity by steam-heat treatment for 20 min at 121 degrees C. Steam-heat treatment for 20 min at 121 degrees C in the absence of surfactant was insufficient to achieve depyrogenation. Polyoxyethylene (9) lauryl ether and decaglycerin mono-laurate similarly enhanced depyrogenation by steam-heat treatment. The effects of all the surfactants were concentration-dependent for all of the six kinds of LPS examined.

Feasibility Studies↗

PubMedDate not supplied

Enhancing effect of nonionic surfactant on the inactivation of lipopolysaccharide by steam-heat treatment II.

n-alkylpolyoxyethylene surfactants (CnH2n+1O(CH2CH2O)mH; CnEm) showed a strong enhancing effect on the inactivation of lipopolysaccharide (LPS) by heat treatment over a wide range of temperatures. The effect of CnE8 (n = 10-16) was observed above the critical micelle concentration (CMC) and above the cloud point, and was influenced by the length of the alkyl chains. The efficacy of the surfactants was in the order C10E8 < C12E8, C16E8 < C14E8. However, the hydrophilic moiety seemed to have no influence. An 80-95% solution of n-butanol showed a similar effect, indicating that LPS was more effectively inactivated in the oily phase of the surfactants than in water. The effect of surfactant on the hydrodynamic diameter of LPS was the same before and after steam-heat treatment for 20 minutes at 121 degrees C. Each surfactant disaggregated LPS without alteration of the activity of LPS before the heat treatment. We consider that the surfactants interact with LPS in the region of lipid A in a manner that favors loss of the activities of LPS during heating.

Chemical Phenomena↗