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http://health.groups.yahoo.com/group/Trying_Low_Oxalates/message/86
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"Where do oxalates come from? Oxalates are present in a lot of plants and fruit that we eat and in virtually all seeds and nuts. Ordinarily, the gut won't absorb much of the oxalate from the diet, and the oxalate will be metabolized by the flora or just leave the body with the stool. Under other conditions, a lot of the dietary oxalate is absorbed. Overabsorption is far more likely to occur when the tight junctions between the cells which line the gut open up and let molecules pass through between the cells in a condition called the "leaky gut" which is similar to a condition in the bladder with open junctions called the "leaky bladder".
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Intestinal microorganisms play a major role in causing the leaky gut. Since SCD greatly reduces the intestinal microorganisms,it is important to read the connection between intestinal permeability and bacteria if we want to heal the leaky gut.
http://archsurg.ama-assn.org/cgi/content/abstract/123/11/1313
Increased intestinal permeability associated with infection in burn patients
T. R. Ziegler, R. J. Smith, S. T. O'Dwyer, R. H. Demling and D. W.
Wilmore
Department of Surgery, Brigham and Women's Hospital, Boston, MA 02215.
Thermal injury may be associated with disruption of normal gut barrier integrity. To test this hypothesis, we assessed intestinal permeability with the nonmetabolizable, poorly absorbed disaccharide lactulose, which is efficiently excluded by the normal intestinal mucosa. Permeability studies were performed in 15 burned patients (aged 18 to 67 years; mean burn size, 40%) and 11 healthy controls. Lactulose, 10 g, was administered enterally, together with 5 g of mannitol as a control, and urinary excretion rates were determined. Lactulose excretion and the lactulose/mannitol excretion ratio increased threefold (160 +/- 30 vs 57 +/- 7 mumol and 0.113 +/- 0.033 vs 0.035 +/- 0.005) in the infected patients (sepsis score, 10 +/- 2; burn size, 38% +/- 6%). In contrast, noninfected burn patients (sepsis score, 0) had permeability values similar to those of controls (66 +/- 10 mumol and 0.036 +/- 0.007). Permeability increased as the severity of infection increased. Infection in burn patients is associated with increased bowel permeability. The intestine may be a primary source of sepsis. Alternatively, the systemic response to infection may alter gut barrier function, which could facilitate translocation of bacteria and absorption of endotoxin.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=Pub
Med&list_uids=8276206&dopt=Citation
1: Gastroenterology. 1994 Jan;106(1):35-41.
The effect of dexamethasone administration on rat intestinal permeability: the role of bacterial adherence.
Spitz J, Hecht G, Taveras M, Aoys E, Alverdy J.
Department of Surgery, University of Illinois, Chicago.
BACKGROUND/AIMS: Previous studies have shown that dexamethasone administration to rats results in diminution of biliary secretory immunoglobulin A concentration and alters intestinal barrier function to bacteria. The aims of this study were to examine and characterize the effect of dexamethasone on intestinal permeability and to determine the possible influence of bacterial adherence to the mucosa in this process. METHODS: Groups of adult Fisher rats were studied, and the effects of dexamethasone administration and bowel decontamination on bacterial adherence and intestinal permeability were determined in various bowel segments. RESULTS: Dexamethasone administration was associated with a significant increase in bacterial adherence to the mucosa, which was most pronounced in the cecum (4.33 +/- 0.2 colony forming units (cfu) (log10) per gram of mucosa for control vs. 6.23 +/- 0.2 for dexamethasone). This was accompanied by significant alterations in intestinal permeability as measured by a decrease in transepithelial electrical resistance (49.5 +/- 4.1 omega.cm2 for control vs. 25.4 +/- 2.5 omega.cm2 for dexamethasone). Dual sodium-mannitol flux analysis showed this defect to be predominantly paracellular. Antibiotic decontamination of the intestine completely abrogated the intestinal permeability defect observed in this model. CONCLUSIONS: Bacterial-mucosal cell interactions may be responsible for alterations in intestinal permeability after dexamethasone administration.
Gastroenterology. 2002 Nov;123(5):1607-15.
* Gastroenterology 2003 Jan;124(1):275. El Asmar Rahzi [corrected to El Asmar Ramzi].
Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure.
El Asmar R, Panigrahi P, Bamford P, Berti I, Not T, Coppa GV, Catassi C, Fasano A.
Department of Pediatrics and Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
BACKGROUND & AIMS: Enteric infections have been implicated in the pathogenesis of both food intolerance and autoimmune diseases secondary to the impairment of the intestinal barrier. On the basis of our recent discovery of zonulin, a modulator of small-intestinal tight junctions, we asked whether microorganisms might induce zonulin secretion and increased small-intestinal permeability. METHODS: Both ex vivo mammalian small intestines and intestinal cell monolayers were exposed to either pathogenic or nonpathogenic enterobacteria. Zonulin production and changes in paracellular permeability were monitored in Ussing chambers and micro-snapwells. Zonula occludens 1 protein redistribution after bacteria colonization was evaluated on cell monolayers. RESULTS: Small intestines exposed to enteric bacteria secreted zonulin. This secretion was independent of either the species of the small intestines or the virulence of the microorganisms tested, occurred only on the luminal aspect of the bacteria-exposed small-intestinal mucosa, and was followed by a decrease in small-intestinal tissue resistance (transepithelial electrical resistance). The transepithelial electrical resistance decrement was secondary to the zonulin-induced tight junction disassembly, as also shown by the disengagement of the protein zonula occludens 1 protein from the tight junctional complex. CONCLUSIONS: This zonulin-driven opening of the paracellular pathway may represent a defensive mechanism, which flushes out microorganisms and contributes to the host response against bacterial colonization of the small intestine.
PMID: 12404235 [PubMed - indexed for MEDLINE]
Surgical stress shifts the intestinal Escherichia coli population to that of a more adherent phenotype: role in barrier regulation.
Rocha F, Laughlin R, Musch MW, Hendrickson BA, Chang EB, Alverdy J.
Department of Surgery, The University of Chicago Medical Center and the Pritzker School of Medicine, Chicago, IL, USA.
BACKGROUND: We have shown that the combination of surgical stress and starvation in mice is associated with a defect in epithelial permeability and increased numbers of mucosa-associated Escherichia coli in the cecum. The aim of this study was to determine the specific role of mucosa-associated E coli on epithelial barrier dysfunction in this model. METHODS: Cecal E coli were harvested from mice 48 hours after a sham operation (control mice) or after a 30% surgical hepatectomy with only water provided ad libitum (short-term starvation) after the surgical procedure. Strains were tested for their ability to adhere to and alter the transepithelial electrical resistance (TEER) of cultured young adult mouse colon epithelial cells. TEER changes were further characterized by mannitol fluxes to confirm a defect in paracellular permeability. RESULTS: Strains of cecal E coli harvested from hepatectomy-starved mice adhered to and altered the permeability of young adult mouse colon cells, whereas E coli from the cecum of control mice were less adherent and had no effect on epithelial permeability. The effect of the strains harvested from mice after hepatectomy on the TEER of young adult mouse colon cells was inhibited by mannose and reversed by ciprofloxacin. CONCLUSION: The combination of surgical stress and short-term starvation is associated with a greater abundance of adherent and barrier-altering strains of E coli in the mouse cecum.
PMID: 11436014 [PubMed - indexed for MEDLINE]
Am J Physiol. 1995 Feb;268(2 Pt 1):G374-9.
Enteropathogenic Escherichia coli adherence to intestinal epithelial monolayers diminishes barrier function.
Spitz J, Yuhan R, Koutsouris A, Blatt C, Alverdy J, Hecht G.
Department of Medicine (Gastroenterology, University of Illinois at Chicago.
The mechanism by which enteropathogenic Escherichia coli (EPEC) causes diarrhea remains elusive. Several alterations within the host cell have been demonstrated to occur following EPEC attachment including increases in intracellular Ca2+ concentration and rearrangement and phosphorylation of several cytoskeletal proteins. The consequences of these intracellular perturbations on host cell function, however, have not been determined. The aim of this study was to examine the effect of EPEC adherence on intestinal epithelial barrier function. T84 cell monolayers were infected with either wild-type EPEC or a nonadherent isogenic derivative. Transepithelial electrical resistance, a measure of barrier function, decreased 33.5 +/- 6.4% after a 6-h incubation with the wild-type strain. Electron microscopy revealed ultrastructurally normal cells, and lactate dehydrogenase release assays failed to demonstrate cytotoxicity. Dual 22Na+ and [3H]mannitol flux studies localized the permeability defect to tight junctions. In addition, cumulative flux of the paracellular marker mannitol was four- to fivefold greater across monolayers infected with wild-type EPEC. Sequestration of intracellular calcium stores by dantrolene completely abrogated the resistance drop associated with EPEC attachment. These data demonstrate that adherence of EPEC to intestinal epithelial cell monolayers disrupts tight junction barrier function via a calcium-requiring event.
PMID: 7864134 [PubMed - indexed for MEDLINE]
The previous article and the next article show that calcium is also helpful for healing intestinal permeability. The SCD yogurt is a wonderful way to get calcium..
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=Pub
Med&list_uids=8574756&dopt=Citation
Shock. 1995 Sep;4(3):204-10.
Exposure of the lateral enterocyte membrane by dissociation of calcium-dependent junctional complex augments endocytosis of enteric bacteria.
Wells CL, van de Westerlo EM, Jechorek RP, Erlandsen SL.
Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis 55455-0374, USA.
Intestinal bacterial translocation is facilitated in a variety of clinical conditions involving increased intestinal permeability, such as shock and trauma. Because there is both in vivo and in vitro evidence that enteric bacteria can be internalized by intestinal epithelial cells, experiments were designed to test the effect of increased intestinal permeability on enterocyte endocytosis of enteric bacteria. Mature, confluent cultures of HT-29 enterocytes were placed in a calcium-free solution for 1 h. Enterocyte viability was not noticeably altered, but transepithelial electrical resistance was significantly decreased (indicating a decrease in epithelial junctional integrity), and the enterocytes were pulled apart. Electron microscopic observations revealed enteric bacteria preferentially adherent on the exposed enterocyte lateral surface, and the numbers of viable enteric bacteria (Listeria monocytogenes, Salmonella typhimurium, Proteus mirabilis, Escherichia coli, and Enterococcus faecalis) internalized by these enterocytes were significantly increased. Restoration of calcium restored confluency to enterocyte cultures, and bacterial internalization reverted to control levels. Thus, calcium-dependent junctional integrity might play a role in augmenting bacterial translocation in clinical conditions associated with increased intestinal permeability.
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