摘要:

Background:In patients with inflammatory bowel disease (IBD), accelerated bone loss and osteopenia have been found. Potential etiologies of these bone abnormalities have included malnutrition, poor calcium intake or absorption, and the use of corticosteroids. Recent studies have suggested that circulating pro-inflammatory cytokines, which are produced in inflamed bowel, can have a profound effect on bone metabolism, particularly bone resorption. Our aim was to characterize the effects of serum from subjects with IBD on bone metabolism in an in vitro bone culture system.Methods:Organ cultures of fetal rat parietal bones were treated with sera from 9 subjects with Crohn's disease, 7 with ulcerative colitis, and 10 controls with functional bowel disease (age range of all subjects 7-16 years). Patients were also classified by disease activity, serum albumin level, erythrocyte sedimentation rate (ESR), and serum interleukin (IL) 6 levels. The effects of sera on bone formation and resorption were quantified.Results:Compared with control serum, serum from patients with Crohn's disease significantly decreased bone dry weight (p < 0.01) and calcium content (p < 0.001) during 96 h of culture, while serum from ulcerative colitis patients had no effect. While no difference in collagen synthesis was noted between any of the three experimental groups, noncollagen protein synthesis was lower in the ulcerative colitis group than in the control group or those with Crohn's disease (p < 0.05). DNA content was similar in all groups. There was no significant effect of serum from any experimental group on bone resorption. There was no demonstrable relationship between clinical disease activity, ESR, or serum IL-6 levels and measures of bone metabolism. Histologic evaluation of cultured bone showed marked differences between control subjects and Crohn's disease patients, with the latter being characterized by disorganization of mineral and osteoid and morphologically abnormal osteoblasts.Conclusions:Serum from children with IBD has a significantly different effect than control serum on an in vitro model of bone metabolism. Our data suggest that circulating factors may affect osteoblasts and bone formation, leading to bone loss. Further work will be required to further characterize the nature of these factors and develop treatment strategies to minimize their effects.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:To evaluate the role of platelet-activating factor (PAF) in a neonatal rat model of necrotizing enterocolitis (NEC).Methods:NEC was reproduced in newborn rats following exposure to formula feeding, asphyxia, and bacterial colonization. The role of endogenous PAF in neonatal NEC was studied by pretreating animals with PAF receptor antagonists (WEB 2170 and WEB 2086) and by measuring intestinal PAF content in animals with NEC, WEB-treated animals, and controls.Results:We found that WEB 2170 (dosed using 10 mg/kg in a.m. and 30 mg/kg in p.m.) markedly reduced the incidence of NEC (3/17 vs. 14/18 control; p < 0.001) and death (6/17 vs. 17/18 control; p < 0.001) compared with saline-treated animals. Although lower WEB 2170 doses prevented NEC, neither fourfold higher dosing with WEB 2170 nor similar dosing with WEB 2086 affected the incidence of disease in this study. PAF content in intestine was elevated in NEC animals (270 ± 80 pg/g) compared with WEB 2170-treated animals (0 pg/g) and maternally fed controls (70 ± 50 pg/g).Conclusions:The data support the role of PAF in the final common pathway of neonatal NEC.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Chronic alcoholism in pregnant animals and humans lead to general growth impairment in their offspring, which show multiple birth defects and delayed grown (fetal alcohol syndrome). Here we study the maturation of the intestine under the effect of chronic exposure to ethanol in utero together with associated malnutrition.Methods:Lactase, acid β-galactosidase, maltase, and alkaline phosphatase activity profiles were monitored in 18-, 19-, 20-, and 21-day-old fetuses from rats kept under three nutritional treatments before and during gestation: alcohol-treated (25% ethanol in drinking water), fiber-treated (50% cellulose-diluted diet) as a control of the malnutrition associated with chronic alcoholism, and control or normal diet. Serum corticosterone determination and lactase immunolocalization were carried out. To detect possible direct effects of ethanol during the period of mucosa development, intestinal explants from 18-, 19-, and 20-day-old control fetuses were cultured either in the basal medium alone or in a medium containing 25 mMethanol for 72, 48, and 24 h of incubation, respectively.Results:Following chronic ethanol exposure in utero, intestinal weight and brush-border protein content and the specific activities of lactase, acid β-galactosidase, maltase, and alkaline phosphatase were significantly lower than those of nutritional controls. Organ culture results, under the assay conditions stated, did not show a direct effect of ethanol 25 mMon prenatal mucosal functionality.Conclusions:All these results suggest that maternal malnutrition is not primarily responsible for the impaired intestinal maturation in rat fetuses from alcohol-treated mothers; indirect effects of ethanol and/or its derivatives throughout embryo-fetal development could be necessary to promote this intestinal delay.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Chronic hepatitis B (CHB) virus infection is associated with functional abnormalities of cell-mediated immunity, defective interferons α and γ synthesis, and interleukin-2 receptor expression. In this study, interleukin-2 (IL-2) production and the role of adherent cells was evaluated in 25 children chronically infected with hepatitis B virus.Methods:IL-2 activity was measured by bioassay in supernatants of phytohemoagglutinin-stimulated peripheral blood mononuclear cells. In a few patients, IL-2 concentration was also immunochemically determined. Coculture experiments using a mixture of adherent cells and lymphocytes from healthy children and patients with CHB were also performed.Results:Children with CHB showed lower IL-2 production than healthy controls. In patients, IL-2 activity was 34.7 ± 22.5 U/ml as compared to 152.6 ± 78.5 U/ml of controls. Immunochemical quantitation of IL-2 confirmed a lower IL-2 production in patients. No correlation was found between the functional T-cell defect and the severity of liver damage, degree of viral replication, and duration of the disease. In co-culture experiments, adherent cells from HBsAg-positive patients inhibited IL-2 production following mitogen stimulation of control non-adherent cells by 67%. The inhibitory effect, mediated by patients' adherent cells, was abolished by blocking with indomethacin prostaglandins, that are potent local immunomodulators released by adherent cells.Conclusions:Our results further support the observation that in children with CHB virus infection, adherent cells play an important role in the inappropriate regulation of immune response, an effect being likely mediated by prostaglandins.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:Previous reports have revealed that fatty liver involving obesity is closely related to insulin resistance or hyperinsulinemia in adulthood. This study investigates the importance of hyperinsulinemia in obese children with fatty liver.Methods:The subjects were 228 obese children 6 to 15 years old in Niigata Prefecture, Japan. The serum level of glutamic pyruvic transaminase (GPT) was evaluated as an indicator of fatty liver. The effects of their percent obesity (percent over ideal body weight), Rohrer index (g/cm3), skinfold thickness, percent body fat measured by bioelectrical impedance analysis, total cholesterol (TC), high-density lipoprotein cholesterol, triglyceride (TG), blood glucose, and immuno-reactive insulin (IRI) on GPT were evaluated using regression analyses.Results:The incidence of fatty liver (GPT over 35 IU/I) was 24.1% in this study. In simple regression analyses, percent obesity, Rohrer index, skinfold thickness, TC, TG, blood glucose, and IRI correlated positively with GPT (p < 0.05). In stepwise regression analysis including these seven variables, the predictive equation for GPT as a function of IRI alone accounted for 24.2% of the total variance of GPT. The addition of TC alone, and TC and percent obesity together increased the coefficients of determination to 28.4% and 29.9%, respectively. Rohrer index, skinfold thickness, Tg, and blood glucose were not taken as related variables with GPT.Conclusion:Hyperinsulinemia is an important contributor to the development of fatty liver, apparently more than anthropometric data, blood glucose, or serum lipids in childhood obesity.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Background:We analyzed the role that nutrition and the insulin-like growth factors IGF-I and IGFBP-3 play on neonatal growth.Methods:Full-term and preterm infants with 1 and 3 weeks of postnatal life (n = 54 and n = 33, respectively) were studied. Anthropmetric variables, daily intake of energy and nutrients, and serum levels of IGF-I and IGFBP-3 were measured.Results:At the first week after birth, preterm infants had lower IGF-I levels than did those in the control group. At the third week of postnatal life, serum IGF-I and IGFBP-3 levels showed a significant increase. Preterm infants born before 33 gestational weeks showed lower IGF-I (p < 0.02) and IGFBP-3 (p < 0.02) levels than those born between 33 and 37 gestational weeks. Preterm infants fed with human milk supplemented with a formula showed higher serum IGF-I levels than those fed exclusively with a milk formula (mean ± SEM 48.2 ± 9.5 μg/L vs. 25.4 ± 4.4 μg/L, p < 0.05). IGF-I and IGFBP-3 were correlated between themselves and with energy and protein intake. Multiple regression analysis confirmed that energy intake and serum IGFBP-3 levels were the most predictable variables with regard to IGF-I levels at neonatal period.Conclusions:These feedings suggest that IGF-I levels during the neonatal periods are influenced by the maturity stage of the newborn, energy intake, and the type of lactation.

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0277-2116    

出版商:OVID    

年代:1997

数据来源: OVID