We examined the correlation between the incidence of Crohn disease and dietary change in a relatively homogeneous Japanese population. The incidence and daily intake of each dietary component were compared annually from 1966 to 1985. The univariate analysis showed that the increased incidence of Crohn disease was strongly (P < 0.001) correlated with increased dietary intake of total fat (r = 0.919). animal fat (r = 0.880), n-6 polyunsaturated fatty acids (r = 0.883), animal protein (r = 0.908), milk protein (r = 0.924), and the ratio of n-6 to n-3 fatty acid intake (r = 0.792). It was less correlated with intake of total protein (r = 0.482, P < 0.05), was not correlated with intake of fish protein (r = 0.055, P > 0.1), and was inversely correlated with intake of vegetable protein (r = -0.941, P < 0.001). The multivariate analysis showed that increased intake of animal protein was the strongest independent factor with a weaker second factor, an increased ration of n-6 to n-3 polyunsaturated fatty acids. The present study in association with reported clinical studies suggests that increased dietary intake of animal protein and n-6 polyunsaturated fatty acids with less n-3 polyunsaturated fatty acids may contribute to the development of Crohn disease.
A number of cell surface proteins have been shown to be anchored to the plasma membrane by a covalently attached glycoinositol phospholipid (GPL) in amide linkage to the C-terminus of the mature protein. We applied several criteria to establish that folate binding protein (FBP) in brush border membranes of rat kidney contains a GPL anchor. Brush border membranes were isolated and labeled with [3H]folate, and the complex of FBP and [3H]folate was shown to be released to the supernatant by incubation with purified bacterial phosphatidylinositol-specific phospholipase C (PIPLC) but not by incubation with a purified bacterial phosphatidylcholine-specific phospholipase C. The FBP-[3H]folate complex both in crude extracts and after FBP purification by ligand-directed affinity chromatography interacted with Triton X-114 micelles, and prior incubation with PIPLC prevented this detergent interaction. Individual residues characteristic of GPL anchors were found to be covalently associated with FBP following polyacrylamide gel electrophoresis in sodium dodecyl sulfate. These included glucosamine and ethanolamine, which were radiolabeled by reductive methylation and identified by chromatography on an amino acid analyzer, and inositol phosphate, which was inferred by Western blotting with an anti-CRD antisera. This antisera gave positive immunostaining only after FBP had been cleaved by PIPLC, a reliable diagnostic of a GPL anchor. The relationship between GPL-anchored FBP in biological membranes and soluble FBP in biological fluids also is discussed.
Red kidney beans were fed to weanling Long-Evans rats to cause diarrhoea (mean (SD) faecal wet weight: 2*66 (0.73) g/day in six rats fed beans v 1*12 (0.47) g/day in six control rats, p<0.01) and increased faecal energy loss (4.87 (0.41) v 2.14 (0.23) kcallday, p<001). In addition, the rats fed beans had heavier small intestines (80.6 (4.6) v 51.9 (8.4) g/kg body weight, p<0.01), heavier mesenteric lymph nodes (0.72 (0.27) 28 days were used. We modified the previously described experimental model, obtaining red kidney beans from a local market as a lectin source and basic rat chow from the Government Flour Mill (Dhaka, Bangladesh).The beans were ground with chow mixed in a ratio of 40:60 as the study diet. For a control diet, ground red kidney beans were autoclaved at 120°C with 1.5 atmospheres for 20 minutes, a procedure known to abolish lectin activity.9 For both control and study diets, calorie densities were 4 kcallg of diet and protein concentrations were 22-24% of total energy.Rats were individually housed in metabolic cages and fasted for 24 hours before the experiment. A pilot study had shown that these rats ate less lectin-containing study diet than control diet. Therefore, six rats in the lectin fed group were pair fed with six controls for the experimental period. The first three days of the study were considered as an equilibrium period. From the fourth to the 10th experimental day, body weight and food consumption were measured, stool was weighed and collected for calorimetry, and faecal energy was measured by an automatic adiabatic bomb calorimeter (Autobomb/Gallenkamp, England).After completing the 10 day metabolic experiment, rats were fasted for 18 hours. Under light ether anaesthesia, using sterile procedures, mesenteric lymph nodes were first collected through a mid-line incision. Then a 10 cm segment of the jejunum below the ligament of Treitz and a 10 cm segment of the ileum proximal to the ileocecal sphincter were collected from each rat. The lumen of each resected segment was rinsed gently with 20 ml of sterile PBS (pH 7.2) which was also collected. Mesenteric lymph nodes, rinsed jejunum and ileum, and PBS washouts were cultured for aerobic bacteria quantitatively using an established technique. 10 Liver, spleen, total small intestine, and mesenteric lymph nodes were weighed and the wet weight of these organs was expressed in g/kg of body weight.Each variable in the lectin fed group was compared with that in the control group by Student's t test. The proportion of lymph nodes from which positive bacterial cultures were obtained were analysed by Fisher's exact test. ResultsAll values are mean (SD) unless otherwise stated. Both the lectin fed and the pair fed control rats lost body weight of a similar magnitude (-13-5 (5.0) v -13-4 (4.4) g/10
ABSTRACT-Prostaglandin (PG) and nitric oxide (NO) have been known to inhibit the lesion formation induced by necrotic agents. However, no clear correlation between PG and NO has been shown in the gastroprotective action against necrotic agent-induced gastric mucosal lesions in rats. Thus, the present study was performed to clarify this correlation. Gastric mucosal lesions were induced by the oral administration of 0.6 M HCl in rats. 16,16-Dimethyl PGE2 (0.3 -3 mg/ kg, p.o.; dim-PGE2), sodium nitrite (0.3 and 1 mg /kg, s.c.) and sodium nitroprusside (30 and 100 m g/kg, i.v.; SNP) dose-dependently inhibited the lesion formation. Orally administered sodium nitrite or SNP (3 mg/kg) also significantly inhibited the lesion formation. The gastroprotective action by dim-PGE 2 was not affected by the pre-treatment with N G -nitro-Larginine methylester (10 mg /kg, i.v.). The gastroprotective effect by sodium nitrite or SNP was markedly attenuated by the pre-treatment with indomethacin (10 mg/ kg, s.c.). These findings suggest that NO donating compounds inhibit the HCl-induced mucosal lesions mainly through prostaglandin, but dim-PGE2 directly inhibits the lesions without involvement of NO in rats.
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