Effects of early feeding and exogenous putrescine on growth and small intestinal development in posthatch ducks.

1. Effects of early feeding with a diet containing added putrescine on duck intestinal development and growth performance were examined by a 2 x 2 factorial arrangement with two different feeding times (6 and 48 h) and two levels of putrescine (0 and 025%). 2. A significant main effect of early feeding on increasing body weight (BW) was observed from hatch to 35 d, whereas dietary putrescine had no significant effect on BW. 3. In the first week posthatch, enhanced small intestinal weight and intestinal density (weight of intestinal tissue/unit length of intestine), increased villus length and reduced crypt depth were observed in the early feeding group, while no effect was observed when putrescine was added to the diet. 4. Maltase and sucrase activity and protein/DNA ratio in jejunum were increased by early feeding in the first week, while decreased by putrescine supplementation. 5. In conclusion, early feeding methods have great potential for small intestine development and thereafter enhanced the growth performance of ducks, but dietary putrescine used during this period should be used cautiously to avoid toxicity.

Acute denervation alters the epithelial response to adrenoceptor activation through an increase in alpha1-adrenoceptor expression on villus enterocytes.

Loss of sympathetic input due to intestinal denervation results in hypersensitivity and increased intestinal secretion. It is unknown whether denervation-induced alterations in intestinal epithelial physiology are the result of changes in adrenoceptors on enterocytes (ENTs). The purpose of this study was to examine adrenoceptor distribution and pharmacology on small intestinal ENTs following acute intestinal denervation. Lewis rats underwent small bowel transplantation (SBT) or sham operation and proximal small intestinal segments were harvested 1, 2 and 4 weeks postoperatively. Intestinal electrolyte movement was assessed using short-circuit current (Isc) measurements of stripped epithelial sheets following stimulation with phenylephrine (PE), an alpha(1)-adrenoceptor agonist. The presence of adrenoceptor subtypes on separated villus and crypt ENTs was assessed using flow cytometry. Alpha(1)-adrenoceptors were found on approximately 27% of jejunal villus ENTs, but not crypt ENTs, following acute extrinsic denervation. ENTs from the Lewis rat have few beta-adrenoceptors. Alpha(1)-adrenoceptor stimulation of acutely denervated intestinal epithelial sheets decreased Isc by -13.45%. This effect was mediated by a reduction in chloride (Cl(-)) secretion; the absence of Cl(-) reversed the Isc to +13.79%. In conclusion, loss of sympathetic innervation to the gastrointestinal epithelium causes acute upregulation of alpha(1)-adrenoceptors on villus ENTs, leading to inhibition of Cl(-) secretion at the villus tip. The increase in adrenoceptors may reflect a compensatory mechanism to combat the increased secretory state of the bowel due to the loss of the sympathetic innervation and tonic control over intestinal secretion.

The significance of gut sucrase activity for osmoregulation in the pea aphid, Acyrthosiphon pisum.

The osmotic pressure of the body fluids of aphids is lower than in their diet of plant phloem sap. It is hypothesised that aphids reduce the osmotic pressure of ingested food by sucrase-mediated hydrolysis of dietary sucrose to glucose and fructose, and the polymerisation of glucose into oligosaccharides of low osmotic pressure per hexose unit. To test this hypothesis, the impact of the alpha-glucosidase inhibitor acarbose on the sugar relations and osmoregulation of aphids was explored. Acarbose inhibited sucrase activity in gut homogenates and the production of monosaccharides and oligosaccharides in the honeydew of live aphids. Acarbose caused an increase in the haemolymph osmotic pressure for aphids reared on a diet (containing 0.75 M sucrose) hyperosmotic to the haemolymph and not on the isoosmotic diet containing 0.2 M sucrose. It did not affect aphid feeding rate over 2 days, except at high concentrations on 0.75 M sucrose diet, and this may have been a secondary consequence of osmotic dysfunction. Acarbose-treated aphids died prematurely. With 5 microM dietary acarbose, mean survivorship on 0.2 M sucrose diet was 4.2 days, not significantly different from starved aphids, indicating that, although these aphids fed, they were deprived of utilisable carbon; and on 0.75 M sucrose diet, mean survivorship was just 2.8 days, probably as a consequence of osmotic failure. It is concluded that the aphid gut sucrase activity is essential for osmoregulation of aphids ingesting food hyperosmotic to their body fluids.

Anti-diarrhoeal and gastro-intestinal potentials of the aqueous extract of Phyllanthus amarus (Euphorbiaceae).

The anti-diarrhoeal and gastro-intestinal protective potentials of aqueous extract of leaves of Phyllanthus amarus were investigated in mice. Graded doses of the aqueous extract (100-800 mg/kg) administered orally produced a dose-related inhibition of gut meal travel distance in normal mice. The highest intestinal transit inhibition of 31.65% was obtained with 400 mg/kg. In castor oil induced diarrhoea in mice, P. amarus extract (400 mg/kg) delayed the onset of diarrhoea, reduced frequency of defecation and reduced gut meal travel distance significantly resulting in intestinal transit inhibition of 79.94% compared to 86.92% produced by morphine (100 mg/kg). In addition, the activities of some intestinal mucosa enzymes (maltase, sucrase, lactase and alkaline phosphatase) in mice pretreated with extract before castor oil were not as severely depressed as those in the control (castor oil treated mice). Phytochemical screening revealed the presence of many secondary metabolites. The results are discussed with a view to establishing the basis of the use of this plant in traditional medicine for treatment of diarrhoea and other gastrointestinal disorders.

Dietary carbohydrate enhances intestinal sugar transport in diabetic mice.

The rate of intestinal absorption of sugars and their site of absorption determine postprandial plasma glucose concentrations. Does chronic consumption of high-carbohydrate, high-fiber, low-fat diets of the type recommended by many diabetes associations induce adaptive changes in transport and metabolism of sugars in the small intestine? Control and STZ-induced diabetic (> 60 days diabetic) mice were fed high-carbohydrate or no-carbohydrate rations for 7 days. Brush-border glucose and fructose uptake per milligram increased 2 times with dietary carbohydrate in both diabetic and control mice; uptake, however, did not differ between diabetic and control mice. Compared with the distal small intestine, glucose uptake per milligram was 2 to 6 times higher in the proximal and middle regions, and enhancement of uptake by diet was limited to these regions. Changes in site density of intestinal glucose transporters as determined by specific phlorizin binding were tightly correlated with changes in brush-border glucose uptake per milligram. There were neither diabetes- nor diet-induced changes in the Kd of specific phlorizin binding, in the amount of glucose absorbed per transporting site, or in passive glucose permeability. Intestinal weights, wt/cm, intestinal length, and mucosal mass increased significantly with diabetes, and sugar transport per centimeter and per small intestine was up to 60% greater in diabetic mice. Dietary carbohydrate stimulated specific sucrase activity in the proximal small intestine of both diabetic and control mice. Chronic diabetes enhances sugar transport by nonspecific increases in intestinal mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of glucose absorption by phlorizin affects intestinal functions in rats.

BACKGROUND: To investigate the mechanism of regulation of intestinal disaccharidase activity and glucose absorption, the effect of dietary intake of phlorizin, a potent and specific inhibitor of intestinal glucose transport, on intestinal disaccharidase activity and Na(+)-dependent glucose transporter was examined in rats. METHODS: Jejunal disaccharidase activity and the number of Na(+)-dependent glucose transporters were determined in rats maintained on a low-starch diet, a high-starch diet, or low-starch diets containing various amounts of phlorizin (0.1%-0.9% wt/wt). RESULTS: Jejunal disaccharidase activity increased in a dose- and time-dependent manner. Stimulation of jejunal disaccharidase activity only occurred when phlorizin was added to starch-containing diets, not when it was added to a carbohydrate-free diet. Addition of the same amount of phloretin and glucose (constituents of phlorizin), to the diet failed to increase disaccharidase activity. The maximum binding of phlorizin to brush border membrane vesicles was increased in the rats fed phlorizin, whereas the dissociation constant remained unchanged, suggesting an increase of glucose transporter expression. CONCLUSIONS: Dietary phlorizin increased the jejunal disaccharidase activity and Na(+)-dependent glucose transporter expression. The trigger for these changes may have been due to an increased luminal glucose content.

Origin and function of the multiple extracellular glucosyltransferase species from cultures of a serotype c strain of Streptococcus mutans.

Two methods were used to purify the bifunctional extracellular enzyme sucrose: (1-6)- and (1-3)-alpha-D-glucan-6-alpha-D-glucosyltransferase (EC 2.4.1.5; dextransucrase) from continuous cultures of a serotype c strain of Streptococcus mutans. The first method, based on a previously published report, involved Sepharose 6B gel filtration and DEAE cellulose anion exchange chromatography. This resulted in a dextransucrase preparation with an apparent molecular mass of 162 kDa and a specific activity of 125 mg of glucan formed from sucrose h-1 (mg of protein)-1, at 37 degrees C. It was almost homogeneous as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The ratio of carbohydrate to protein was 0.14 and the recovery was 14% relative to the total glucosyltransferase activity in the original culture fluid. In the subsequently preferred method, hydroxyapatite-Ultrogel was used to purify dextransucrase with a 24% yield. The specific activity, 197 mg of glucan formed h-1 (mg of protein)-1, was the highest yet reported and this preparation contained less than 0.5 glucose-equivalent per subunit of molecular mass 162 kDa. Dextransucrase is therefore not a glycoprotein. Exogenous dextran stimulated activity, but was not essential for activity. The purified protein slowly degraded to multiple lower molecular mass forms during storage at 4 degrees C and 87% of the activity was lost after 20 days. The molecular mass of the most prominent, active degradation product was 140 kDa, similar to that of one of the multiple forms of dextransucrase detected in other laboratories. Preparations in which either the 140-kDa or the 162-kDa species predominated catalyzed the synthesis of a water-soluble glucan with sucrose alone, but catalyzed that of an insoluble glucan with sucrose and a high concentration of either (NH4)2SO4 or polyethylene glycol. The water-insoluble glucan was shown to lack sequences of 1,3-alpha-linked glycosyl residues typical of the insoluble glucan, mutan, which has been implicated in dental caries. We conclude that mutan is synthesized by the concerted action of two independent glucosyltransferases rather than by interconvertible forms of a single enzyme, as was proposed previously.

Thyroxin-evoked increase of sucrase activity in lower villus in the jejunum of adrenalectomized suckling rats.

Intestinal sucrase activity, absent in the suckling rat, is evoked precociously by thyroid hormones. Since enterocytes migrate from crypt to villus tip, the question arises: at which level of the villus--crypt columns do the enterocytes respond with an increase of sucrase activity to thyroxin (T4)? Suckling rats (11 days old) were injected daily, subcutaneously, with T4 (2 micrograms/g BW/day). They were sacrificed 1, 2, and 3 days later. Sucrase activity was determined in homogenates of the entire jejunal wall and in serial homogenates of the villus-crypt columns using cryostat sectioning. Maximal increase of sucrase activity was seen after 3 days in the lower villus. Experiments were also done using rats adrenalectomized on day 10 to exclude the effect via precocious maturation of adrenal cortex. The same results were obtained. In conclusion, T4-evoked increase of sucrase activity occurs first in enterocytes that are nearest the villus-crypt junction.

A -D-fructofuranosidase from Claviceps purpurea.

Evidence suggests that sucrose is the main carbon source for growth of Claviceps spp. in the parasitic condition. The sucrose acts as substrate for an active beta-fructofuranosidase, produced by the fungus, which in the first instance converts the disaccharide into glucose and an oligofructoside. In this way, 50% of the glucose, supplied as sucrose, is made available to the parasite for assimilation. Subsequent action of the enzyme on both sucrose and the oligofructoside leads to the release of more glucose and the formation of additional oligosaccharides. The structures of the main oligosaccharides formed have been elucidated and the interactions of each compound studied. In experiments with purified enzyme in vitro the interaction of the oligosaccharides is rapid but in culture they are assimilated only slowly; in each case some free fructose is liberated. Free fructose is not assimilated in the presence of glucose and, further, inhibits growth at concentrations which might be expected to occur in the parasitic condition. A dual role has been suggested for the enzyme, with sucrose as substrate, in which glucose is made available to the growing parasite, while at the same time transfer of the fructose to form oligosaccharides prevents it from accumulating at inhibitory concentrations. Ultimately, when glucose becomes limiting, the fungus will adapt to fructose assimilation.