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Dominik Linz - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of Sodium-proton-exchanger subtype 3-mediated Sodium Absorption in the gut: A new antihypertensive concept.
International journal of cardiology. Heart & vasculature, 2020Co-Authors: Benedikt Linz, Mathias Hohl, Michael Bohm, Arnela Saljic, Thomas Jespersen, Prashanthan Sanders, Monika Gawałko, Dominik LinzAbstract:Abstract Arterial hypertension is one of the main contributors to cardiovascular diseases, including stroke, heart failure, and coronary heart disease. Salt plays a major role in the regulation of blood pressure and is one of the most critical factors for hypertension and stroke. At the individual level, effective salt reduction is difficult to achieve and available methods for managing Sodium balance are lacking for many patients. As part of the ingested food, salt is absorbed in the gastrointestinal tract by the Sodium proton exchanger subtype 3 (NHE3 also known as Slc9a3), influencing extracellular fluid volume and blood pressure. In this review, we discuss the beneficial effects of pharmacological inhibition of NHE3-mediated Sodium Absorption in the gut and focus on the effect on blood pressure and end-organ damage.
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Pharmacological inhibition of Sodium-proton-exchanger subtype 3-mediated Sodium Absorption in the gut reduces atrial fibrillation susceptibility in obese spontaneously hypertensive rats.
International journal of cardiology. Heart & vasculature, 2020Co-Authors: Benedikt Linz, Mathias Hohl, R. Mishima, Arnela Saljic, Dennis H. Lau, Thomas Jespersen, Ulrich Schotten, Prashanthan Sanders, Dominik LinzAbstract:Abstract Background Increased Sodium uptake has been shown to contribute to hypertension and cardiac end-organ damage. The Sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal Sodium Absorption. Whether a reduction in intestinal Sodium Absorption can prevent the development of an atrial arrhythmogenic substrate in hypertension is unknown. Methods Eight-week-old obese spontaneously hypertensive rats (SHR-ob) were treated for six weeks with the gut-specific NHE3-inhibitor SAR (1-(β-D-glucopyranosyl)-3-{3-[(4S)-6,8-dichloro-2-methyl-1,2,3,4-tetrahydroiso-chinolin-4-yl]phenyl}urea, 1 mg/kg/d in chow, SHR-ob SAR, n = 7) and compared to aged-matched placebo-treated SHR-ob (SHR-ob PLAC, n = 8). Cardiac magnetic resonance imaging was performed at the end of the treatment period to assess atrial emptying function. Afterwards, local conduction disturbances and inducible atrial fibrillation (AF) duration were determined and histological analysis to quantify atrial fibrosis amount were performed. Results Inhibition of intestinal NHE3 by SAR increased fecal Sodium excretion, resulted in marked changes in feces electrolyte concentrations and water content, reduced blood pressure and preserved atrial emptying function (active total percent emptying: SHR-ob SAR: 0.47 ± 0.05% vs. SHR-ob PLAC: 0.38 ± 0.007, p Conclusions Reduction of intestinal Sodium Absorption and subsequent changes in feces milieu by pharmacological NHE3 inhibition in the gut preserved atrial emptying function and reduced AF susceptibility. Whether pharmacological NHE3 inhibition in the gut prevents AF in humans warrants further study.
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inhibition of nhe3 mediated Sodium Absorption in the gut reduced cardiac end organ damage without deteriorating renal function in obese spontaneously hypertensive rats
Journal of Cardiovascular Pharmacology, 2016Co-Authors: Benedikt Linz, Mathias Hohl, Jan Christian Reil, Michael Bohm, Dominik LinzAbstract:Abstract:Increased Sodium Absorption in the gut is one mechanism contributing to hypertensive blood pressure values. The Sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal Sodium Absorption. The compound SAR is a new specific NHE3 inhibitor with extremely low oral absorb
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Inhibition of NHE3-mediated Sodium Absorption in the Gut Reduced Cardiac End-organ Damage Without Deteriorating Renal Function in Obese Spontaneously Hypertensive Rats.
Journal of cardiovascular pharmacology, 2016Co-Authors: Benedikt Linz, Mathias Hohl, Jan Christian Reil, Michael Bohm, Dominik LinzAbstract:Increased Sodium Absorption in the gut is one mechanism contributing to hypertensive blood pressure values. The Sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal Sodium Absorption. The compound SAR is a new specific NHE3 inhibitor with extremely low oral absorbability leading to decreased Sodium Absorption in the gut and substantial systolic blood pressure reduction. The effects of intestinal NHE3 inhibition on cardiac and renal hypertensive end-organ damage are unknown. The effects of SAR (1 mg·kg⁻¹·d⁻¹ in chow) on left ventricular (LV) and renal remodeling processes were studied by magnetic resonance imaging and biochemical and histological analysis in obese spontaneously hypertensive rats (SHR-ob SAR) compared with placebo-treated SHR-ob (SHR-ob PLAC). Inhibition of intestinal NHE3 by SAR lowered blood pressure and reduced LV end-diastolic pressure from 21 ± 3.0 to 15 ± 2.0 mm Hg (P = 0.0016), whereas heart rate kept unchanged. LV mass indices, LV myocyte diameters, and LV fibrosis formation were lower in SHR-ob SAR compared with SHR-ob PLAC. SAR did not influence urinary albumin to creatinine ratio or glomerular filtration rate. Renal interstitial fibrosis formation, as well as podocyte damage and glomerulosclerosis remained unchanged. Reduction of intestinal Sodium Absorption by selective NHE3 inhibition in the gut lowered high blood pressure and reduced LV remodeling without deteriorating renal functional and structural parameters in SHR-ob.
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Antihypertensive and Laxative Effects by Pharmacological Inhibition of Sodium-Proton-Exchanger Subtype 3–Mediated Sodium Absorption in the Gut
Hypertension (Dallas Tex. : 1979), 2012Co-Authors: Dominik Linz, Klaus Wirth, Wolfgang Linz, Hubert Otto Heuer, Wendelin Frick, Armin Hofmeister, Uwe Heinelt, Petra Arndt, Uwe Schwahn, Michael BohmAbstract:High intestinal Sodium Absorption is one mechanism of hypertension and constipation. The Sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of Sodium Absorption in the gut. SAR218034 (SAR) is an orally nonabsorbable specific NHE3 inhibitor. The effect of SAR (1 mg/kg per day in chow) on feces Sodium excretion, systolic blood pressure via tail cuff, and gene expression of NHE3 in the gut were studied in senescent lean hypertensive rats (spontaneously hypertensive rats-lean, loaded with NaCl 0.7% in drinking water) and in hypertensive, obese, and hyperinsulinemic rats (spontaneously hypertensive rats-obese, not loaded with NaCl). In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces Sodium excretion and reduced urinary Sodium excretion, whereas absolute Sodium balance and serum Sodium concentration were not changed. This suggests reduced intestinal Sodium Absorption in SAR-treated animals and was associated with increased feces water content (58% versus 42% in placebo treated animals; P =0.0001) and reduction in systolic blood pressure from 222±7 to 198±2 mm Hg ( P =0.0001). Angiotensin-converting enzyme inhibition by ramipril plus NHE3 inhibition resulted in an additive blood pressure–lowering effect. In spontaneously hypertensive rats-obese, SAR lowered systolic blood pressure but did not modify serum insulin or cholesterol levels. Gene expression of NHE3 was upregulated in the ileum and colon but not in the jejunum of SAR-treated rats. Reduction of intestinal Sodium Absorption by selective NHE3 inhibition in the gut reduces high blood pressure and increases feces water excretion. Intestinal NHE3 blockade could be a new treatment strategy for elderly patients suffering from high blood pressure and constipation.
Jörg-dieter Schulzke - One of the best experts on this subject based on the ideXlab platform.
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Glucocorticoids and Tumor Necrosis Factor-α Synergize to Induce Absorption by the Epithelial Sodium Channel in the Colon
Gastroenterology, 2008Co-Authors: Theresa Bergann, Sebastian Zeissig, Anja Fromm, Michael Fromm, Jan F. Richter, Jörg-dieter SchulzkeAbstract:Background & Aims The epithelial Sodium channel (ENaC) mediates electrogenic Sodium Absorption in distal colon. In patients with inflammatory bowel disease (IBD), ENaC induction is impaired, mainly through transcriptional suppression by proinflammatory cytokines such as tumor necrosis factor (TNF)-α. Glucocorticoid therapy rapidly increases Sodium Absorption; we investigated the molecular mechanisms underlying the interaction among TNF-α, glucocorticoids, and ENaC induction. Methods ENaC-mediated Sodium transport in glucocorticoid receptor (GR)-expressing HT-29/B6 cells and rat distal colon, under the influence of the synthetic glucocorticoid dexamethasone and TNF-α, was quantified in Ussing chambers. ENaC messenger RNA (mRNA) levels were monitored by real-time polymerase chain reaction. GR transactivation and expression were investigated by gene reporter, immunoblot, and confocal immunofluorescence microscopy analyses. The GR mRNA half-life was determined. Signaling pathways were characterized using mitogen-activated protein kinase inhibitors. Results Dexamethasone not only prevented TNF-α-mediated ENaC suppression but caused synergistic induction of ENaC-dependent Sodium Absorption in HT-29/B6-GR cells and rat distal colon. This synergy resulted from TNF-α-mediated increases in GR protein levels because of GR mRNA stabilization and subsequent GR transactivation by dexamethasone. As a consequence, transcription of the ENaC β- and γ-subunits was up-regulated, increasing ENaC-dependent Sodium Absorption. p38 Mitogen-activated protein kinase is required for this synergistic effect: p38 inhibition blocked the increase in GR protein expression and ENaC-dependent Sodium Absorption. Conclusions TNF-α and dexamethasone induce ENaC, explaining the rapid and intense proabsorptive effect of glucocorticoid therapies.
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Altered ENaC expression leads to impaired Sodium Absorption in the noninflamed intestine in Crohn's disease.
Gastroenterology, 2008Co-Authors: Sebastian Zeissig, Theresa Bergann, Anja Fromm, Christian Bojarski, Frank Heller, Ute Guenther, Martin Zeitz, Michael Fromm, Jörg-dieter SchulzkeAbstract:Background & Aims: Crohn's disease (CD) is a chronic inflammatory bowel disease. In this study, we have investigated Sodium Absorption via epithelial Sodium channels (ENaC) in the macroscopically noninflamed colon in active CD. Methods: Sodium transport via ENaC was investigated in Ussing chambers using biopsy specimens of sigmoid colon from controls and active CD limited to the small intestine. ENaC messenger RNA expression and subcellular localization were studied by real-time polymerase chain reaction and confocal microscopy. Effects of proinflammatory cytokines on ENaC and signaling via mitogen-activated protein kinases were investigated in rat distal colon. Therapeutic inhibition of mitogen-activated protein kinases was studied in CD biopsy specimens. Results: Electrogenic Sodium Absorption via ENaC was strongly impaired in the macroscopically noninflamed CD colon because of reduced γ-ENaC transcription, whereas subcellular localization of ENaC was not changed. In contrast to impaired epithelial Sodium transport, epithelial barrier function was not altered in noninflamed CD colon, indicating that paracellular leak flux of ions did not contribute to decreased Sodium Absorption. Exposure of rat distal colon to tumor necrosis factor α led to reduced electrogenic Sodium Absorption because of impaired transcriptional γ-ENaC induction, which resembled the changes found in CD. Tumor necrosis factor α effects were dependent on extracellular signal-regulated kinase 1/2 but not p38 or c-Jun-N-terminal kinase because inhibition of mitogen-activated protein kinase/extracellular regulated kinase (MEK)1/2 but not inhibition of p38 or c-Jun-N-terminal kinase prevented suppression of ENaC. Finally, therapeutic inhibition of MEK1/2 restored electrogenic Sodium Absorption in CD. Conclusions: In CD, macroscopically noninflamed colon contributes to diarrhea via impaired ENaC-mediated Sodium Absorption. Inhibition of extracellular signal-regulated kinase might serve as a potential therapeutic strategy for CD diarrhea.
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Butyrate induces intestinal Sodium Absorption via sp3-mediated transcriptional up-regulation of epithelial Sodium channels
Gastroenterology, 2007Co-Authors: Sebastian Zeissig, Anja Fromm, Martin Zeitz, Michael Fromm, Joachim Mankertz, Jörg Weiske, Jörg-dieter SchulzkeAbstract:Background & Aims: The epithelial Sodium channel (ENaC) is the rate-limiting factor for colonic electrogenic Sodium Absorption. This study aimed to investigate ENaC regulation by butyrate, a short-chain fatty acid (SCFA) produced by intestinal bacteria. Methods: ENaC was examined in HT-29/B6 cells and glucocorticoid receptor(GR)-transfected HT-29/B6 cells (HT-29/B6-GR) by reverse-transcription polymerase chain reaction, real-time polymerase chain reaction, and confocal microscopy. ENaC promoters were investigated by deletion/mutation analysis, electrophoretic mobility shift assays, and quantitative chromatin immunoprecipitation. Sodium transport of HT-29/B6-GR cells and rat distal colon was quantified in Ussing chambers. Results: Butyrate up-regulated β- and γ-ENaC mRNA expression in HT-29/B6 cells and induced transcription from β- and γ-ENaC promoter constructs. The γ-ENaC promoter could also be induced by the SCFA propionate but not by acetate. Deletion/mutation assays revealed that activation of the γ-ENaC promoter depended on 2 GC boxes, which were shown to bind Sp1 and Sp3 in vitro. Although both transcription factors increased butyrate-mediated γ-ENaC transcription upon overexpression, chromatin immunoprecipitation revealed that only Sp3 binds to the γ-ENaC promoter in vivo and that Sp3 binding is enhanced by butyrate. Transcriptional ENaC induction by butyrate led to synthesis of γ-ENaC subunits, but correct targeting of ENaC channels to the apical cell membrane was dependent on corticosteroid hormones. Finally, butyrate substantially increased electrogenic Sodium Absorption via ENaC in the presence of corticosteroid hormones in HT-29/B6-GR cells and in rat distal colon. Conclusions: Concerted action of SCFA and corticosteroid hormones is required for induction of ENaC and maintenance of intestinal electrogenic Sodium Absorption.
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IL-1β and TNFα regulate Sodium Absorption in rat distal colon
Biochemical and biophysical research communications, 2004Co-Authors: Christian Barmeyer, Martin Zeitz, Michael Fromm, Joachim Mankertz, Salah Amasheh, Shida Tavalali, Jörg-dieter SchulzkeAbstract:Abstract The epithelial Na+ channel (ENaC) provides the main absorptive pathway of the distal large intestine. This study aimed to characterize regulatory influences of cytokines in rat late distal colon. After 6 h incubation with either IL1β, TNFα, IFNγ, or combinations of TNFα and IFNγ, ENaC was measured as electrogenic Na+ transport after 8 h induction by 3 nM aldosterone (JNa) in totally stripped specimens in the Ussing chamber. Subsequently, α-, β-, and γ-ENaC subunit mRNAs were analyzed by Northern blotting. The γ-ENaC promoter was cloned and characterized by reporter gene assays. IL-1β and TNFα, but not interferon-γ, decreased JNa. In parallel, β- and γ-ENaC transcription was inhibited, whereas α-ENaC was unaffected. γ-ENaC promoter activity was inhibited by IL-1β and TNFα but not by IFNγ. We conclude that the pro-inflammatory cytokines IL-1β and TNFα inhibit electrogenic Sodium Absorption in rat distal colon by mRNA expression regulation of the β- and γ-ENaC subunits.
Jacques Cosnes - One of the best experts on this subject based on the ideXlab platform.
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effects of an isotonic oral rehydration solution enriched with glutamine on fluid and Sodium Absorption in patients with short bowel syndrome
Alimentary Pharmacology & Therapeutics, 1997Co-Authors: Laurent Beaugerie, J. P. Gendre, F Carbonnel, B Hecketsweiler, P Dechelotte, Jacques CosnesAbstract:AIM To compare the effects of a standard oral rehydration solution with a polymeric glucose isotonic solution enriched with glutamine on water and Sodium Absorption in the short bowel. METHODS Six patients with high jejunostomy were tested in a random order on 2 consecutive days with the standard solution (20 g/L glucose, 94 mmol/L Sodium, 292 mOsm/kg osmolality) and a solution containing maltodextrins (18 g/L Glucidex 12; hydrolysis of 18 g of Glucidex 12 yields 20 g glucose) enriched with 14.6 g/L of glutamine (94 mmol/L Sodium, 282 mOsm/kg osmolality). Solutions were administered via a naso-gastric tube at a rate of 2 mL/min. Jejunal effluent for each solution was collected during an 8-h period, after a 14-h equilibrium period. RESULTS The net 8-h fluid Absorption was not significantly different between the standard solution and the solution with glutamine (333 +/- 195 and 213 +/- 251 mL, respectively (mean +/- S.E.M.)). Net Sodium Absorption was higher for the standard solution than for the solution with glutamine (15 +/- 15 vs. 2 +/- 20 mmol, P < 0.05). The rate of glucose Absorption was not different between the solutions. CONCLUSION The replacement of glucose by maltodextrins and the addition of glutamine to the standard oral rehydration solution, without changing its Sodium content or osmolality, results in a reduction of Sodium Absorption in the short-bowel syndrome.
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Effects of an isotonic oral rehydration solution, enriched with glutamine, on fluid and Sodium Absorption in patients with short‐bowel syndrome
Alimentary pharmacology & therapeutics, 1997Co-Authors: Laurent Beaugerie, J. P. Gendre, F Carbonnel, B Hecketsweiler, P Dechelotte, Jacques CosnesAbstract:AIM To compare the effects of a standard oral rehydration solution with a polymeric glucose isotonic solution enriched with glutamine on water and Sodium Absorption in the short bowel. METHODS Six patients with high jejunostomy were tested in a random order on 2 consecutive days with the standard solution (20 g/L glucose, 94 mmol/L Sodium, 292 mOsm/kg osmolality) and a solution containing maltodextrins (18 g/L Glucidex 12; hydrolysis of 18 g of Glucidex 12 yields 20 g glucose) enriched with 14.6 g/L of glutamine (94 mmol/L Sodium, 282 mOsm/kg osmolality). Solutions were administered via a naso-gastric tube at a rate of 2 mL/min. Jejunal effluent for each solution was collected during an 8-h period, after a 14-h equilibrium period. RESULTS The net 8-h fluid Absorption was not significantly different between the standard solution and the solution with glutamine (333 +/- 195 and 213 +/- 251 mL, respectively (mean +/- S.E.M.)). Net Sodium Absorption was higher for the standard solution than for the solution with glutamine (15 +/- 15 vs. 2 +/- 20 mmol, P < 0.05). The rate of glucose Absorption was not different between the solutions. CONCLUSION The replacement of glucose by maltodextrins and the addition of glutamine to the standard oral rehydration solution, without changing its Sodium content or osmolality, results in a reduction of Sodium Absorption in the short-bowel syndrome.
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Isotonic high-Sodium oral rehydration solution for increasing Sodium Absorption in patients with short-bowel syndrome.
American Journal of Clinical Nutrition, 1991Co-Authors: Laurent Beaugerie, Jacques Cosnes, F. Verwaerde, H. Dupas, P. Lamy, J. P. Gendre, Y. Le QuintrecAbstract:We compared the effect of a standard oral rehydration solution and a high-Sodium polymeric-glucose solution on Sodium Absorption in short-bowel syndrome. Six patients with high jejunostomy were tested in a random order with the standard solution or a solution containing maltodextrins (18 g Glucidex 12/L) enriched with 2.5 g NaCl/L. Solutions were administered via a nasogastric tube at a rate of 2 mL/min. Jejunal effluent was collected during an 8-h period. The net 8-h fluid Absorption was not significantly different in the two periods. Glucose Absorption was greater than 90% of the administered amount for both solutions. Net Sodium Absorption was greater for the maltodextrin solution than for the standard solution (56 +/- 12 vs 24 +/- 20 mmol, P less than 0.05). We conclude that replacement of glucose with maltodextrins and addition of Sodium in the standard oral rehydration solution results in improved Sodium Absorption in short-bowel syndrome.
Eun Young Jung - One of the best experts on this subject based on the ideXlab platform.
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analysis of the effects of biopolymer encapsulation and Sodium replacement combination technology on the quality characteristics and inhibition of Sodium Absorption from sausage in mice
Food Chemistry, 2018Co-Authors: Eun Young JungAbstract:Abstract The effects of biopolymer encapsulation and Sodium replacement combination technology on quality characteristics (i.e., bitter taste) and inhibition of Sodium Absorption from pork sausage in mice were evaluated. The sausages were divided into three different Sodium replacement groups (none, 40%, and 50%) and three different biopolymer encapsulation groups (none, cellulose, and chitosan) in combination. In groups with 50% Sodium replacement by KCl and MgCl2, T8 (chitosan encapsulation) showed the highest inhibition of the Sodium Absorption rate. However, chitosan encapsulation groups (T2, T5, and T8) had higher bitterness and lower overall acceptability than other treatment groups. In contrast, in the group with 40% Sodium replacement by KCl, T4 (cellulose encapsulation) exhibited the highest inhibition of Sodium Absorption without a bitter taste. This is the first report showing that 40–50% Sodium replacement combined with 3% cellulose encapsulation reduced Sodium Absorption from sausage by 60% without causing a bitter taste.
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Development of Sausage with Inhibition of 60% Sodium Intake, Using Biopolymer Encapsulation Technology and Sodium Replacers
Food and Bioprocess Technology, 2018Co-Authors: Eun Young JungAbstract:To develop sausage with inhibition of 60% Sodium intake, using biopolymer encapsulation technology and Sodium replacer, the sausages were subdivided into five treatment groups: control was the normal Sodium amount without Sodium substitution and biopolymers; and four treatments involved encapsulation with four different biopolymers (T1: pectin, T2: chitosan, T3: cellulose, T4: dextrin), with Sodium substituted by 55% with Sodium replacers (a mixture of potassium, magnesium, and calcium chlorides). The experimental sausages were fed to mice for 48 h, and Sodium Absorption and its inhibition were measured. T2 sausage (3% chitosan with a Sodium replacer) and T3 sausage (3% cellulose with a Sodium replacer) showed the highest rates of inhibition of Sodium Absorption: 69.65 and 67.34%, respectively. These results indicated that the final goal of 60% inhibition of Sodium intake was accomplished by 55% Sodium replacement and more than 15% inhibition of Sodium Absorption with minimal deterioration of sausage quality.
Laurent Beaugerie - One of the best experts on this subject based on the ideXlab platform.
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effects of an isotonic oral rehydration solution enriched with glutamine on fluid and Sodium Absorption in patients with short bowel syndrome
Alimentary Pharmacology & Therapeutics, 1997Co-Authors: Laurent Beaugerie, J. P. Gendre, F Carbonnel, B Hecketsweiler, P Dechelotte, Jacques CosnesAbstract:AIM To compare the effects of a standard oral rehydration solution with a polymeric glucose isotonic solution enriched with glutamine on water and Sodium Absorption in the short bowel. METHODS Six patients with high jejunostomy were tested in a random order on 2 consecutive days with the standard solution (20 g/L glucose, 94 mmol/L Sodium, 292 mOsm/kg osmolality) and a solution containing maltodextrins (18 g/L Glucidex 12; hydrolysis of 18 g of Glucidex 12 yields 20 g glucose) enriched with 14.6 g/L of glutamine (94 mmol/L Sodium, 282 mOsm/kg osmolality). Solutions were administered via a naso-gastric tube at a rate of 2 mL/min. Jejunal effluent for each solution was collected during an 8-h period, after a 14-h equilibrium period. RESULTS The net 8-h fluid Absorption was not significantly different between the standard solution and the solution with glutamine (333 +/- 195 and 213 +/- 251 mL, respectively (mean +/- S.E.M.)). Net Sodium Absorption was higher for the standard solution than for the solution with glutamine (15 +/- 15 vs. 2 +/- 20 mmol, P < 0.05). The rate of glucose Absorption was not different between the solutions. CONCLUSION The replacement of glucose by maltodextrins and the addition of glutamine to the standard oral rehydration solution, without changing its Sodium content or osmolality, results in a reduction of Sodium Absorption in the short-bowel syndrome.
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Effects of an isotonic oral rehydration solution, enriched with glutamine, on fluid and Sodium Absorption in patients with short‐bowel syndrome
Alimentary pharmacology & therapeutics, 1997Co-Authors: Laurent Beaugerie, J. P. Gendre, F Carbonnel, B Hecketsweiler, P Dechelotte, Jacques CosnesAbstract:AIM To compare the effects of a standard oral rehydration solution with a polymeric glucose isotonic solution enriched with glutamine on water and Sodium Absorption in the short bowel. METHODS Six patients with high jejunostomy were tested in a random order on 2 consecutive days with the standard solution (20 g/L glucose, 94 mmol/L Sodium, 292 mOsm/kg osmolality) and a solution containing maltodextrins (18 g/L Glucidex 12; hydrolysis of 18 g of Glucidex 12 yields 20 g glucose) enriched with 14.6 g/L of glutamine (94 mmol/L Sodium, 282 mOsm/kg osmolality). Solutions were administered via a naso-gastric tube at a rate of 2 mL/min. Jejunal effluent for each solution was collected during an 8-h period, after a 14-h equilibrium period. RESULTS The net 8-h fluid Absorption was not significantly different between the standard solution and the solution with glutamine (333 +/- 195 and 213 +/- 251 mL, respectively (mean +/- S.E.M.)). Net Sodium Absorption was higher for the standard solution than for the solution with glutamine (15 +/- 15 vs. 2 +/- 20 mmol, P < 0.05). The rate of glucose Absorption was not different between the solutions. CONCLUSION The replacement of glucose by maltodextrins and the addition of glutamine to the standard oral rehydration solution, without changing its Sodium content or osmolality, results in a reduction of Sodium Absorption in the short-bowel syndrome.
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Isotonic high-Sodium oral rehydration solution for increasing Sodium Absorption in patients with short-bowel syndrome.
American Journal of Clinical Nutrition, 1991Co-Authors: Laurent Beaugerie, Jacques Cosnes, F. Verwaerde, H. Dupas, P. Lamy, J. P. Gendre, Y. Le QuintrecAbstract:We compared the effect of a standard oral rehydration solution and a high-Sodium polymeric-glucose solution on Sodium Absorption in short-bowel syndrome. Six patients with high jejunostomy were tested in a random order with the standard solution or a solution containing maltodextrins (18 g Glucidex 12/L) enriched with 2.5 g NaCl/L. Solutions were administered via a nasogastric tube at a rate of 2 mL/min. Jejunal effluent was collected during an 8-h period. The net 8-h fluid Absorption was not significantly different in the two periods. Glucose Absorption was greater than 90% of the administered amount for both solutions. Net Sodium Absorption was greater for the maltodextrin solution than for the standard solution (56 +/- 12 vs 24 +/- 20 mmol, P less than 0.05). We conclude that replacement of glucose with maltodextrins and addition of Sodium in the standard oral rehydration solution results in improved Sodium Absorption in short-bowel syndrome.