Acute effect of ethanol on intestinal calcium transport.

Krishnamra, Nateetip; Boonpimol, Pornpimol

doi:10.3177/jnsv.32.229

Cited by 6 publications

(2 citation statements)

References 23 publications

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“…Since the colon is a site of calcium absorption rather than calcium secretion (20,21), the endogenous calcium present in the colon probably resulted from a transit from the distal small intestine. Consistent with our previous in situ investigation (3), the present in vivo study demonstrated that ethanol markedly stimulates gastric calcium secretion and suppresses calcium absorption in the proximal small intestine (Fig. 5).…”

Section: Discussionsupporting

confidence: 93%

The in vivo effect of ethanol on gastrointestinal motility and gastrointestinal handling of calcium in rats.

Krishnamra

Limlomwongse

1987

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe acute effects of an intragastric administration of ethanol (2g/kg body weight) (given as 13.3% w/v solution) on the in vivo gastrointestinal motility and gastrointestinal absorption and secretion of calcium were investigated in 20-h fasted rats. Gastric ethanol con centration remained high for 90min while the concentration in the duodenum peaked at 30min before declining to a range slightly higher than that in the mid and distal intestine. Plasma ethanol peaked at 60min. From the polyethylene glycol (PEG) distribution, ethanol was found to delay gastric emptying, and at 60min, 40% of PEG was still retained in the stomach of the ethanol-treated group while gastric emptying had been completed in the controls. However, ethanol placed directly into the duodenum was found to enhance intestinal motility.Under control conditions, exogenous calcium was completely ab sorbed by the time it reached the mid-small intestine (J3) and calcium found in more distal segments was of endogenous origin. Ethanol sup pressed calcium absorption while markedly stimulating calcium secretion in the stomach and the distal small intestine, resulting in a net 32% in crease in the total gastrointestinal calcium content. This effect on the distal small intestine was from ethanol that had reached this area from the circulation, and not from ethanol transit along the gastrointestinal tract.

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Section: Discussionsupporting

confidence: 93%

The in vivo effect of ethanol on gastrointestinal motility and gastrointestinal handling of calcium in rats.

Krishnamra

Limlomwongse

1987

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Recent experiments from our laboratory showed that a short duodenal exposure (30 min) of 15% alcohol by volume (ABV) induce low-grade morphological changes in only a small number of duodenal villi tips in rats [5]. Additionally, ethanol induces dysmotility, increases duodenal epithelial paracellular permeability, and stimulates gastric acid secretion as well as pancreatic exocrine secretion [6], [7], [8], [9].…”

Section: Introductionmentioning

confidence: 99%

The Ethanol-Induced Stimulation of Rat Duodenal Mucosal Bicarbonate Secretion In Vivo Is Critically Dependent on Luminal Cl–

et al. 2014

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Alcohol may induce metabolic and functional changes in gastrointestinal epithelial cells, contributing to impaired mucosal barrier function. Duodenal mucosal bicarbonate secretion (DBS) is a primary epithelial defense against gastric acid and also has an important function in maintaining the homeostasis of the juxtamucosal microenvironment. The aim in this study was to investigate the effects of the luminal perfusion of moderate concentrations of ethanol in vivo on epithelial DBS, fluid secretion and paracellular permeability. Under thiobarbiturate anesthesia, a ∼30-mm segment of the proximal duodenum with an intact blood supply was perfused in situ in rats. The effects on DBS, duodenal transepithelial net fluid flux and the blood-to-lumen clearance of 51Cr-EDTA were investigated. Perfusing the duodenum with isotonic solutions of 10% or 15% ethanol-by-volume for 30 min increased DBS in a concentration-dependent manner, while the net fluid flux did not change. Pre-treatment with the CFTR inhibitor CFTRinh172 (i.p. or i.v.) did not change the secretory response to ethanol, while removing Cl− from the luminal perfusate abolished the ethanol-induced increase in DBS. The administration of hexamethonium (i.v.) but not capsazepine significantly reduced the basal net fluid flux and the ethanol-induced increase in DBS. Perfusing the duodenum with a combination of 1.0 mM HCl and 15% ethanol induced significantly greater increases in DBS than 15% ethanol or 1.0 mM HCl alone but did not influence fluid flux. Our data demonstrate that ethanol induces increases in DBS through a mechanism that is critically dependent on luminal Cl− and partly dependent on enteric neural pathways involving nicotinic receptors. Ethanol and HCl appears to stimulate DBS via the activation of different bicarbonate transporting mechanisms.

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