The BB rat spontaneously develops autoimmune diabetes. Feeding these animals a hydrolyzed casein diet significantly reduces the incidence of this disease, suggesting that a dietary antigen is involved in the pathogenesis of this disease. In other syndromes associated with luminal antigens, including celiac and Crohn’s disease, increased intestinal permeability has been suggested to play an etiological role. Therefore, the objective of this study was to evaluate whether increased permeability was also present in BB rats before disease development. By measuring gastrointestinal permeability, in animals on a regular or hydrolyzed casein diet, we were able to demonstrate that increased gastric and small intestinal permeability appeared before the development of both insulitis and clinical diabetes. Although hydrolysis of dietary protein significantly reduced the incidence of diabetes, it did not alter the small intestinal permeability abnormality, suggesting that this is an early event. Increased permeability appears to have an early role in the genesis of several immunological diseases and may represent a common event in these diseases.

Colitis is associated with alterations in electrolyte and water transport. These changes give rise to some of the symptoms experienced by patients with colitis. Alterations in fluid flux may also contribute to increased susceptibility to mucosal injury. Recently, endogenous water channel proteins (aquaporins; AQPs), have been identified in colonic tissue. The expression of AQP4, AQP7 and AQP8 was examined, via reverse transcription/polymerase chain reaction, Western blotting and immunohistochemistry, in a murine model of colitis and in patients with inflammatory bowel disease or infectious colitis. Colitis was induced in C57BL/6 mice by the addition of 2.5% dextran sodium sulphate (DSS) to their drinking water. AQP expression in these mice was assessed following 12 h to 7 days of DSS exposure and during the recovery phase from 1 to 15 days following cessation of DSS exposure. Colonic water transport was measured after 1 and 3 days of DSS and following 7 days of recovery. The expression of AQP4 and AQP8 mRNA was significantly decreased after 12-24 h of DSS exposure and remained depressed throughout the treatment period. Expression of AQP7 was more variable. Protein expression followed a similar pattern to that observed for AQP mRNA. Significant alteration in colonic fluid secretion was correlated with reduced expression of AQP isoforms. Significantly, patients with active ulcerative colonic, Crohn's colitis or infectious colitis had similar dramatic reductions in AQP expression that appeared to be correlated with disease activity. Thus, colonic injury in both mouse and man is associated with a downregulation in AQP expression.

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The role of epidermal growth factor (EGF) in the acute regulation of intestinal transport of electrolytes and glucose was examined. In vivo transport studies were performed in New Zealand White rabbits (500-900 g) using a single-pass perfusion technique. In vitro net fluxes were determined under short-circuited conditions in Ussing chambers. Kinetic parameters of glucose transport in the presence and absence of EGF were measured in brush-border membrane vesicles. In vivo studies showed that the addition of 60 ng/ml EGF to the perfusate resulted in increased absorption of H2O, Na+, Cl-, and glucose from the jejunum. In Ussing chambers, the presence of EGF caused an increase in jejunal net fluxes of glucose-stimulated Na+ and 3-O-methylglucose due to an increase in mucosal-to-serosal movements. Verapamil abolished the EGF effect. In the absence of glucose, net fluxes of Na+ and Cl- were enhanced in the presence of EGF due to a decrease in the serosal-to-mucosal movement of both ions. Verapamil had no effect on this decrease. The incubation of EGF with brush-border membrane vesicles had no effect on either the maximal flux or the Michaelis constant of glucose transport. These results indicate that EGF is capable of regulating absorption of electrolytes and nutrients from the small intestine and suggest a role for this peptide in the control of intestinal transport.

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Aim-We examined the eVect of proinflammatory and anti-inflammatory interleukins on jejunal nutrient transport and expression of the sodium-glucose linked cotransporter (SGLT-1). Methods-3-O-methylglucose and L-proline transport rates were examined in New Zealand White rabbit stripped, short circuited jejunal tissue. The eVects of the proinflammatory cytokines interleukin (IL)-1 , IL-6, and IL-8, IL-1 plus the specific IL-1 antagonist, IL-1ra, and the anti-inflammatory cytokine IL-10 were investigated. In separate experiments, passive tissue permeability was assessed and brush border SGLT-1 expression was measured by western blot in tissues exposed to proinflammatory interleukins. Results-The proinflammatory interleukins IL-6, IL-1 , and IL-8 significantly increased glucose absorption compared with control levels. This increase in glucose absorption was due to an increase in mucosal to serosal flux. IL-1 and IL-8 also significantly increased L-proline absorption due to an increase in absorptive flux. The anti-inflammatory IL-10 had no eVect on glucose transport. The receptor antagonist IL-1ra blocked the ability of IL-1 to stimulate glucose transport. IL-8 had no eVect on passive tissue permeability. SGLT-1 content did not diVer in brush border membrane vesicles (BBMV) from control or interleukin treated tissue. Conclusions-These findings suggest that intestinal inflammation and release of inflammatory mediators such as interleukins increase nutrient absorption in the gut. The increase in glucose transport does not appear to be due to changes in BBMV SGLT-1 content.

Field experiments were conducted in steel bins containing 13,600 kg of hard red winter wheat, Triiticum aestivum L. One bin was treated with ozone and the second bin served as a control. Stored grain insects were placed in bins for 1-, 2-, 3-, and 4-d exposure periods in sampling tubes to test ozone concentrations of 0, 25, 50, and 70 parts per million by volume (ppmv). Ozone treatments on eggs and larvae of Plodia interpunctella (Hübner) were not effective, but pupae were more susceptible. Sitophilus oryzae (L.) adults were the most susceptible species with 100% mortality reached after 2 d in all ozone treatments. However, some progeny were produced at all concentrations and exposure periods. Tribolium castaneum (Herbst) adults had 100% mortality only after 4 d at 50 or 70 ppmv. No T. castaneum progeny were produced after 2-4 d at 70 ppmv. For Rhyzopertha dominica (F.), Cryptolestes ferrugineus (Stephens), and Oryzaephilus surinamensis (L.), 100% mortality was never achieved and progeny were produced at all ozone concentrations. Laboratory experiments, testing the effectiveness of ozone in controlling psocids, were conducted in two polyvinyl chloride cylinders each containing 55 kg of hard red winter wheat. Ozone treatment at a concentration of 70 ppmv was highly effective against adult female Liposcelis bostrychophila Badonnel and Liposcelis paeta Pearman after only 1 d of exposure. However, it was not effective against eggs of both species at all exposure periods. Ozonation has potential for the control of some stored grain insect pests on wheat.

Na+-glucose cotransporter (SGLT1) expression and the role of actin in epidermal growth factor (EGF)-induced alterations in glucose transport and brush-border surface area were examined in New Zealand White rabbit jejunal loops. In separate experiments, EGF or EGF concurrent with cytochalasin D, an inhibitor of actin polymerization, was administered to the experimental loop and compared with its vehicle control. SGLT1 expression was measured by Western blot in brush-border membrane vesicles (BBMV) after 5-min and 1-h exposure. Glucose kinetics were determined by a rapid filtration technique, and brush-border surface area was examined by electron microscopy after 1-h exposure. The effect of cytochalasin D alone on BBMV glucose kinetics and brush-border surface area was also assessed. EGF resulted in a significant increase in BBMV SGLT1 expression ( P < 0.05), glucose maximal uptake ( V max; P < 0.001), and absorptive brush-border surface area ( P < 0.001). These effects were abolished with concurrent cytochalasin D treatment. Cytochalasin D alone had no effect on glucose transport or brush-border surface area. The findings suggest that EGF acutely upregulates jejunal brush-border surface area and the V max for jejunal glucose uptake via the recruitment and insertion of SGLT1 from an internal pool into the brush border by a mechanism that is dependent on actin polymerization.