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At least 1,063 records · Page 59Linked to original sources
PubMed1992

Nutritional support in inflammatory bowel disease: current status and future directions.

Malnutrition is a frequent occurrence in patients with acute inflammatory bowel disease. Total nutritional support provided either parentally (TPN) or enterally (TEN) has been advocated not only as an adjunct for improving nutrition but also as primary therapy. For patients with acute Crohn's disease, short-term rates of remission after TEN are equivalent to TPN. Coupled with certain advantages when compared with TPN, including simpler administration, fewer side effects, and preservation of the intestinal mucosal barrier, TEN may therefore be the preferred route for nutrient delivery. Controlled trials indicate equivalent or superior efficacy when enteral polymeric diets are compared with elemental diets for inducing remission in acute Crohn's disease. Moreover, when provided as an elemental diet, TEN is as effective as corticosteroids for achieving remission in acute Crohn's disease, but corticosteroids appear to be more effective than polymeric diets. Although the provision of nutritional support rather than bowel rest is the major factor contributing to symptomatic improvement, the optimal nutrient composition and the precise mechanisms whereby nutritional support achieves clinical remission remain to be clarified. In contrast to Crohn's disease, nutritional support is not effective for achieving remission in patients with ulcerative colitis. Thus, enteral nutritional support is an effective therapy for the short-term management of acute Crohn's disease. Whether long-term remission is equivalent to treatment with drugs or surgery requires prospective evaluation. Future avenues of investigation also include defining the optimal nutrient composition and the underlying mechanisms that achieve maximal nutritional repletion, promote mucosal cell renewal, and potentially directly retard production of inflammatory mediators.

Crohn Disease↗
PubMed1994

ADSA Foundation Lecture. Low calcium intake: the culprit in many chronic diseases.

Calcium is the fifth most abundant element in the earth's crust and is necessary for both plant and animal life today. Moreover, the natural diets of all mammals are rich in calcium. The diet of Stone Age human adults is estimated to have contained from 50 to 75 mmol of calcium (2000 to 3000 mg)/d, three to five times the median calcium intake of present-day US adults. Human physiology has adapted to this environmental abundance with an intestinal absorptive barrier and inefficient renal conservation of calcium. Although mammalian physiology contains mechanisms by which organisms can adjust to temporary environmental shortages, chronic calcium retention has a number of health consequences, most notably bone fragility, high blood pressure, and colon cancer. Evidence indicates that improvement in calcium intake (or in vitamin D status) prevents some portion of each of these multifactorial problems. At least 14 intervention studies have established the skeletal benefit of increased calcium intake during growth and among women in the late postmenopause. Other evidence suggests that adequate calcium may protect against salt-sensitive and pregnancy-associated hypertension and that high intakes of both dietary calcium and vitamin D reduce development of precancerous changes in colonic mucosa.

Calcium↗
PubMed2002

Effects of recombinant human growth hormone on rat septic shock with intraabdominal infection by E. coli.

AIM: To investigate the therapeutic effects of recombinant human growth hormone (rhGH) on rat septic shock with intraabdominal infection by E. coli and its possible mechanism. METHODS: 76 SD rats were divided into 3 groups randomly: control group (group C, n=16) without any special treatment, septic shock group (group S, n=30) received bolus injection of E.coli (1X10(10) cfu x L(-1), 15 ml x kg(-1), ip), treated group (group T, n=30) received bolus injection of E.coli, and then followed by rhGH injection (2.25 U x k g(-1) x d(-1), im). Group S and group T were further divided into 1d and 3d subgroups, respectively (n=15 each). Mean arterial pressure (MAP), levels of plasma TNFalpha and endotoxin and leukocyte count were determined on 1st day and 3rd day after E.coli injection. Another 39 SD rats were divided into groups C, S and T (n=13 each) just for observing survival rate within 1 week. RESULTS: (1) On 1st and 3rd day, MAP in group S decreased markedly, and MAP on 1st day lowered more than that of 3rd day (P<0.01), while MAP in group T just decreased slightly. The survival rate within 1 week was much higher in group T (84.6 %) than in group S (46.2 %) (P<0.01). (2)On 1st day, plasma TNFalpha and endotoxin elevated significantly in group S and group T (P<0.05), and endotoxin in group S had more increase (P<0.01). On 3rd day, TNFagr in group S returned to the level of group C (P>0.05),while TNFagr in group T went down below the level of group C(P<0.01). On 3rd day, endotoxin in group S declined, but was still higher than that of group C (P<0.01), endotoxin in group T returned to the level of group C (P>0.05). (3) On 1st day, neutrophil ratio in total leukocyte count in both group S and group T increased significantly (P<0.05 vs group C). CONCLUSION: rhGH showed beneficial effects on rat septic shock. The possible mechanisms may involve the attenuation of bacteria/endotoxin translocation and decreased systemic endotoxin level; inhibition of the production and release of TNFalpha; improved circulatory function; improved systemic host defenses and maintenance of intestinal mucosa barrier.

Abdomen↗
PubMed2003

[Alcoholic liver disease].

Ethanol toxicity on liver is a function of duration of alcoholism, amount of daily intake of alcohol and patient's nutrition. The threshold of alcohol toxicity on the liver is about 40 g of ethanol daily in men and 20-30 g in women, however liver cirrhosis develops in no more than 8-20% of patients exceeding this values. Ethanol is oxidized in the liver to acetaldehyde--a compound considerably more toxic than ethanol itself. Despite small amount of alcohol dehydrogenase (ADH) found in gastric mucosa, the metabolism of ethanol in this site may have an important hepatoprotective effect. The oxidation of ethanol is associated with a change of hepatocyte redox homeostasis, which leads to a number of metabolic disorders such as lactic acidosis, hyperlipidaemia and hyperuricaemia. Chronic ethanol consumption does not influence ADH activity, but has a profound stimulatory effect on microsomal enzymes, in particular cytochrome CYP2E1. This fact is responsible for development in alcoholic liver associated with rise of oxygen consumption, excessive production of free radicals and increased metabolism of ethanol, vitamin A and testosterone. Ethanol and acetaldehyde have a deleterious effect, both the direct and indirect, on hepatocytes e.g., generating radical oxygen species and damaging intestinal mucosal barrier. Cellular oxidative stress that is caused by both an excess of free radicals and the antioxidatives' deficiency (glutathion, vitamin E, phosphatidylcholine), may be the principal factor responsible for progression of alcoholic liver disease. Among other factors accelerating alcohol-related liver lesion there are certain drugs, high fat diet, infection with HCV and genetic factors (female sex, enzymatic polymorphic forms of ADH and ALDH, hemochromatosis). Great importance in pathogenesis of necrotic and inflammatory hepatic events is being attributed to portal endotoxaemia and cytokines induced within the liver, in particular TNF-alpha and interleukin 8. These cytokines play a key role in development of alcoholic hepatitis, which clinical severity ranges from subclinical to fatal forms. Apart from abstinence, the treatment of alcohol liver disease is based on hyperalimentation, since alcoholism is generally associated with protein malnutrition. In severe forms of alcohol hepatitis corticosteroids are recommended.

Alcoholism↗
PubMed1992

[New findings in emergency care and resuscitation in patients at risk for endotoxic shock].

Endotoxin shock is not only the reflexion of Gram-negative focal infection but also the consequence of dysfunction of the intestinal mucous barrier and a decline of the detoxication capacity, in particular of the hepatic mesenchymal phagocytic system during a critical state. Cytokines and the primary LPS complex and its lipid A resp. are of basic importance. They start the release of a large amount of TNF alpha, IL-1, IL-6, IL-8 and other cascades. Acute shock is controlled nowadays more frequently than in the past, however, there is a high risk of a very adverse reaction of remote organs, which is very adverse from the prognostic aspect. A series of laboratory markers has a greater validity than the clinical picture alone. For screening derived markers are used not primary markers. Despite this they provide adequate information. Prophylaxis and treatment include selective bacterial decontamination, or active or passive immunization (PSAEVA, hyperimmune sera), minidoses of dopamine in a continuous infusion, early enteral nutritional intervention, in particular enteral nutrition containing glutamine. Monoclonal and polyclonal antibodies against the LPS complex and cytokines are tested, blocking their receptors or possibly early plasmapheresis. Permanent pillars of therapeutic tactics are still a radical and early elimination of possible infectious foci and targeted administration of antibiotics and maintenance of the perfusion pressure and adequate oxygenation.

Humans↗
PubMed2006

[Mechanism of oral absorption of panaxnotoginseng saponins].

AIM: To study the mechanism of absorption after oral administration of panaxnotoginseng saponins (PNS). METHODS: Caco-2 cells and rat models were applied to evaluate the degradation of both ginsenoside Rb1 (Rb1) and ginsenoside Rg1 (Rg1) in PNS in gastrointestinal lumen, and the transport mechanism of PNS across the intestinal mucosa, and the barrier function of stomach, intestine and liver involved in absorption process. RESULTS: Rb1 and Rg1 proved to be readily eliminated in stomach, but stable in relatively neutral circumstance. Both Rb1 and Rg1 in PNS, especially for Rb1, degraded significantly in the contents of large intestine. However, both of them kept mainly intact in the contents of small intestine. Uptake of both Rb1 and Rg1 by Caco-2 cell monolayer was inhibited at low temperature, but not by cyclosporine A, and the change in the apical pH showed no pronounced effect. Uptake and transport were non-saturable and increased linearly with increasing of concentrations of Rb1 and Rg1 over the range of concentration tested, which indicated a passive transport. There was no significant difference of absorption characteristic between monomer (Rb1 and Rg1) and mixture (PNS). Uptake amount of Rg1 [(1.07 +/- 0.16) microg x mg(-1) (protein)] (C0 = 1 mg x mL(-1)) in Caco-2 cells was a little higher than that of Rb1 [(0.77 +/- 0.03) microg x mg(-1) (protein)] (C0 = 1 mg x mL(-1)). Meanwhile, apparent permeability coefficient of (5.9 +/- 1.0) x 10(-8) cm x s(-1) (C0 = 1 mg x mL(-1)) for Rb1 and (2.59 +/- 0.17) x 10(-7) cm x s(-1) (C0 = 1 mg x mL(-1)) for Rg1 from apical compartment to basolateral compartment predicted an incompletely absorption. Transports of both Rb1 and Rg1 were not influenced by cyclosporine A. The investigation on the pharmacokinetic behavior of Rb1 and Rg1 after different routes of administration to rats showed that the absolute bioavailability after peroral (po), intraduodenal (id), and portal venous (pv) administration is 0.71% , 2.75% and 65.77% respectively for Rb1, and 3.29%, 6.60% and 50.56% respectively for Rg1. CONCLUSION: Transport across Caco-2 cell monolayer for PNS (include Rb1 and Rg1) is a simple passive diffusion process. No efflux transporters in Caco-2 cells and other components in PNS showed effects on it. The elimination in stomach, large intestine and liver contributed to the low bioavailability of PNS, but the low membrane permeability might be a more important factor dominating the extent of absorption.

Administration, Oral↗
PubMedDate not supplied

Bacterial translocation from the gut: a mechanism of infection.

Bacterial infection is a common and serious problem in burn victims who survive the shock phase of thermal injury. Our experimental work, plus the clinical studies of others, suggests that the gut can serve as a reservoir for systemic infections caused by bacteria that cross (translocate) the gastrointestinal (GI) epithelium. Bacterial translocation from the GI tract does not normally occur in the healthy animal owing to (1) the presence of an indigenous GI microflora preventing bacterial overgrowth, (2) an intact intestinal epithelial barrier, and (3) normal host immune defenses. However, a thermal injury, as well as other stressors, can result in the disruption or impairment of any of these protective mechanisms, potentially leading to lethal systemic infections with bacteria colonizing the gut.

Animals↗
PubMed1994

Inflammatory bowel disease: diagnosis and treatment.

The primary feature of IBD which distinguishes pediatric from adult patients is the presence of or potential for significant growth failure. Recognizing this complication before permanent stunting occurs is critically important. The onset of these disorders during childhood also means that many of these children will have a lifetime of disease and therapy, during both growing as well as reproductive years. The impact of this lifelong process on the psychosocial development of the child and adolescent also needs to be recognized and addressed. Treatments must be carefully considered for their chronic adverse consequences (side effects) as well as immediate benefits. This includes the risks of early, and likely repeated, bowel resections as well as potentially mutagenic or teratogenic medications. The resurgence of tuberculosis and other chronic intestinal infections, particularly in certain high-risk pediatric populations, requires a careful consideration of the differential diagnosis of IBD in children. Finally, promising therapies must be tested in children as well as adults to develop the most effective approach to controlling IBD in pediatric patients by taking advantage of potential age-related differences in intestinal immune barrier function.

Child↗
PubMed1977

Hepatic reticuloendothelial protection against bacteremia in experimental hemorrhagic shock.

Gram-negative septicemia is an increasingly common problem, and various suggestions have been made about the cause. One not often considered is that it may be the result of failure of hepatic removal of organisms which have crossed the intestinal mucosal barrier from the large bowel lumen to the portal blood stream. Splanchnic hypoperfusion both increases mucosal permeability and reduces the ability of the hepatic reticuloendothelial system (RES) to remove particulate matter from the blood. If RES funciton is reduced further by blockade with colloidal carbon, then any tnedency for bacteremia to occur in shock might be enhanced. Splenectomized greyhounds, who had received a portal perfusion of either colloidal carbon or saline, were subjected to a period of hypovolemia and then were resucitated. Peripheral blood cultures were sterile at all times in the control animals and before bleeding in the dogs that recived carbon. However, all the RE-blockaded animals developed bacteremia during shock, It was condluded that hepatic RES funciton was essential in the prevention of bacteremia in the hypovolemic dog and that investigation should be directed toward studies of RES function in man with a view to determining the importance or otherwise of the RES in relation to gram-negative bacteremia.

Animals↗
PubMed1996

[Observation and analysis of postburn changes in substance P (SP) and SP peptidergic nerve fibers in the intestine of rat].

Substance P (SP) was measured by radioimmunoassay (RIA) and SP peptidergic nerve fibers were identified by Immunohistochemistry (IHC) in the intestinal wall of rats (TBSA 30% and with full-thickness burn) during 72 hours after burn. The results were as follows: (1) SP increased significantly at 1 hr and 4 hr postburn, then decreased markedly 8 hr later, and the low was maintained up to 72 hr. (2) The significant changes in SP peptidergic nerve fibers in the villi after burn were found with immunohistochemical studies including the morphology, distributive densities and SP contents of the SP peptidergic nerve fibers. The results from image analysis showed that the distributive densities of the nerve fibers elevated distinctly in 1 hr group, then dropped at 8 hr and 12 hr and finally elevated again. The results indicated that, the SP release might occur leading to SP consumption in the intestinal wall of rats after burn. It is possible that SP contributes to the postburn intestinal lesion in rats. The SP peptidergic nerve fibers in villus have a direct effect on the damage of intestinal mucosal barrier.

Animals↗
PubMed1998

[Metabolism and nutritional support after burn injury].

The nutritional status of the burn patient plays a major role in the ability to ward off an infectious challenge. The immune and inflammatory systems can be modulated by nutritional support, and therefore this article focuses on the nutritional support after burn injury. The hypermetabolic response that occurs after burn injury is characterized by a greater magnitude than that observed after any other form of trauma. The hypothesis that gut-or wound-derived bacterial translocation is one of the major triggers of the hypermetabolic response has attracted attention recently. The first set of goals of nutritional support is to prevent starvation and nutrient deficiencies, and the second is to provide the correct amount of nutrients prevent injury-related adverse physiologic complications. The route and timing of nutritional support are most important. Enteral alimentation appears to preserve the host immune function and to attenuate the hypermetabolic response by preserving the intestinal mucosal barrier. Immediate enteral feeding is superior to delayed enteral feeding, even though only limited amounts of enterally administered nutrients are absorbed during the early days postburn.

Bacterial Infections↗
PubMed1996

[Intestinal cytokine liberation after intestinal ischemia in the rat--studies in the Ussing chamber system].

UNLABELLED: Intestinal ischemia, frequently found in clinical states such as aortic bypass operations or hemorrhagic shock, is associated with loss of gut barrier function. Subsequent translocation of indigenous bacteria and endotoxin have been implicated as a major contributor to a systemic immuno-inflammatory response, which finally leads to multiple organ failure. There is increasing evidence that intestinal injury can result in the gut becoming a cytokine generating organ. This study was designed to show direct evidence of the gut as a major source of proinflammatory cytokines after intestinal ischemia and to further relate this cytokine response to the extent of intestinal ischemia/reperfusion. Additionally the potential role of the altered intestinal barrier function after intestinal ischemia for this cytokine response was investigated. METHODS: Rats were subjected to occlusion of the superior mesenteric artery for 45 min. (SMAO45), 75 min. (SMAO75), SMAO for 45 min. and 30 min. reperfusion (SMAO45/30), or sham SMAO, and then killed. Mucosal membranes from the terminal ileum were mounted in a Ussing chamber. E. coli C25 was added to the mucosal side of the stripped gut epithelium in half of the chambers. TNF and IL-6 levels on mucosal and serosal side of the stripped gut epithelium were assessed serially over 3 hrs. Gut barrier function was assessed by in vitro bacterial translocation (BT) and the transepithelial resistance (TER) of the mucosal membrane. RESULTS: The TNF response was greatest in the SMAO75 group, the IL-6 response in the SMAO75 and SMAO45/30 groups. In the absence of E. coli C25. IL-6 was produced to a greater extent on the serosal side, while addition of bacteria led to a significantly increased TNF/IL-6 response at the mucosal side of the stripped gut epithelium. BT was increased in SMAO75 and SMAO45/30 rats. Baseline TER was decreased in all experimental compared to sham SMAO groups. Although gut barrier function was impaired after intestinal ischemia/reperfusion there was no correlation between intestinal cytokine response and gut permeability. CONCLUSIONS: The gut becomes a cytokine liberating organ alter intestinal ischemia/reperfusion. This cytokine response is affected by certain conditions, but is not directly related to an impaired intestinal barrier function.

Animals↗
PubMed2003

Migration of Toxoplasma gondii across biological barriers.

The molecular mechanisms underlying migration of pathogens across biological barriers remain poorly characterized. Following oral infection, the apicomplexan parasite Toxoplasma gondii actively crosses non-permissive biological barriers such as the intestine, the blood-brain barrier and the placenta, thereby gaining access to tissues where it causes severe pathology. Recently, enhanced migration was found to be associated with virulent strains of Toxoplasma, suggesting that this phenotype contributes to pathogenesis. The migratory machinery appears to be morphologically and functionally well conserved within the phylum of apicomplexan parasites, however, the mechanisms for cellular traffic to breach biological barriers remain to be elucidated. As penetration of host tissue is a prerequisite for the establishment of infections by most apicomplexan parasites, understanding parasite migration is crucial for the development of new approaches to combat disease.

Actin Cytoskeleton↗
PubMed2001

Prediction of intestinal absorption and blood-brain barrier penetration by computational methods.

This review surveys the computational methods that have been developed with the aim of identifying drug candidates likely to fail later on the road to market. The specifications for such computational methods are outlined, including factors such as speed, interpretability, robustness and accuracy. Then, computational filters aimed at predicting "drug-likeness" in a general sense are discussed before methods for the prediction of more specific properties--intestinal absorption and blood-brain barrier penetration--are reviewed. Directions for future research are discussed and, in concluding, the impact of these methods on the drug discovery process, both now and in the future, is briefly considered.

Animals↗
PubMed2002

Acidomucin goblet cell expansion induced by parenteral nutrition in the small intestine of piglets.

Total parenteral nutrition (TPN) impairs small intestine development and is associated with barrier failure, inflammation, and acidomucin goblet cell expansion in neonatal piglets. We examined the relationship between intestinal goblet cell expansion and molecular and cellular indices of inflammation in neonatal piglets receiving TPN, 80% parenteral + 20% enteral nutrition (PEN), or 100% enteral nutrition (control) for 3 or 7 days. Epithelial permeability, T cell numbers, TNF-alpha and IFN-gamma mRNA expression, and epithelial proliferation and apoptosis were compared with goblet cell numbers over time. Epithelial permeability was similar to control in the TPN and PEN jejunum at day 3 but increased in the TPN jejunum by day 7. By day 3, intestinal T cell numbers were increased in TPN but not in PEN piglets. However, goblet cell expansion was established by day 3 in both the TPN and PEN ileum. Neither TNF-alpha nor IFN-gamma mRNA expression in the TPN and PEN ileum correlated with goblet cell expansion. Thus goblet cell expansion occurred independently of overt inflammation but in association with parenteral feeding. These data support the hypothesis that goblet cell expansion represents an initial defense triggered by reduced epithelial renewal to prevent intestinal barrier failure.

Animals↗