GALACTOSE TRANSPORT ACROSS RAT SMALL INTESTINE <i>IN VIVO</i> FOLLOWING DISTAL RESECTIONS OF VARYING EXTENTS

Bolufer, J; Delgado, Ma José; Murillo, Francisco J.; Murillo, María Luisa Ojeda

doi:10.1113/expphysiol.1986.sp003001

Cited by 8 publications

(3 citation statements)

References 25 publications

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“…This is accompanied by a increased paracellular flux without any significant change in net transluminal or transepithelial glucose flux. The point at which paracellular glucose flux and SGLT1 flux are equal lies between 20 and 30 mM as has been previously observed 4 – 6 . This value is used as one of the key registration points for the model.…”

Section: Discussionsupporting

confidence: 75%

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Does apical membrane GLUT2 have a role in intestinal glucose uptake?

Naftalin

2014

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It has been proposed that the non-saturable component of intestinal glucose absorption, apparent following prolonged exposure to high intraluminal glucose concentrations, is mediated via the low affinity glucose and fructose transporter, GLUT2, upregulated within the small intestinal apical border.The evidence that the non-saturable transport component is mediated via an apical membrane sugar transporter is that it is inhibited by phloretin, after exposure to phloridzin. Since the other apical membrane sugar transporter, GLUT5, is insensitive to inhibition by either cytochalasin B, or phloretin, GLUT2 was deduced to be the low affinity sugar transport route.As in its uninhibited state, polarized intestinal glucose absorption depends both on coupled entry of glucose and sodium across the brush border membrane and on the enterocyte cytosolic glucose concentration exceeding that in both luminal and submucosal interstitial fluids, upregulation of GLUT2 within the intestinal brush border will usually stimulate downhill glucose reflux to the intestinal lumen from the enterocytes; thereby reducing, rather than enhancing net glucose absorption across the luminal surface.These states are simulated with a computer model generating solutions to the differential equations for glucose, Na and water flows between luminal, cell, interstitial and capillary compartments. The model demonstrates that uphill glucose transport via SGLT1 into enterocytes, when short-circuited by any passive glucose carrier in the apical membrane, such as GLUT2, will reduce transcellular glucose absorption and thereby lead to increased paracellular flow. The model also illustrates that apical GLUT2 may usefully act as an osmoregulator to prevent excessive enterocyte volume change with altered luminal glucose concentrations.

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Section: Discussionsupporting

confidence: 75%

“…The apparent transport parameters (K m and V max ) 4 – 6 obtained. In intestinal enterocytes in situ , where flows with varying luminal glucose concentrations are normally measured in steady state, have scant resemblance to those obtained in zero-trans conditions with isolated membrane vesicles or oocytes.…”

Section: Discussionmentioning

confidence: 99%

Does apical membrane GLUT2 have a role in intestinal glucose uptake?

Naftalin

2014

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“…After intestinal resection or bypass (BP) changes in intestinal structure and function occur affecting hormonal regulation or nutritional state of the organism [2,3,6,13,27].…”

Section: Introductionmentioning

confidence: 99%

Comparative effect of distal and proximal intestinal resection and bypass on the rat exocrine pancreas

et al. 1990

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We studied the effects of small-bowel resection and bypass on pancreatic function in rats subjected to a 50% distal resection (DR), a 50% proximal resection (PR), a 50% jejunal bypass (BP) or an intestinal transection (SH) (controls). Duodenal contents were collected after cannulation (under basal conditions). Afterwards, an in vivo duodenal perfusion was made using a glucose/saline solution and perfusate was collected for 1 h. Following this, a cholecystokinin (CCK) solution was injected into the jugular vein (1 U/kg body wt.) and perfusion continued for another 1 h. Basal duodenal volume only increased in rats with a PR, and no significant changes occurred in protein content. In basal conditions, no decreases in amylase, lipase, trypsin, or chymotrypsin activities after DR, PR or BP were detected. When animals were subjected to a perfusion and CCK stimulation, no significant changes occurred in animals with BP; the volume was maintained in rats with PR and DR but a decrease in protein and enzymatic contents was found. We concluded that, in basal conditions, the lack (resections) or exclusion (BP) of 50% of the small bowel does not negatively affect the digestive function. When however, a sustained activity is required, the extirpation of intestinal surface provokes a fall in enzymatic activities and is not modified if only the intestinal transit is suppressed, as occurs in the cases of BP.

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Contribution of solvent drag through intercellular junctions to absorption of nutrients by the small intestine of the rat

1987

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The lumen of the small intestine in anesthetized rats was recirculated with 50 ml perfusion fluid containing normal salts, 25 mM glucose and low concentrations of hydrophilic solutes ranging in size from creatinine (mol wt 113) to Inulin (mol wt 5500). Ferrocyanide, a nontoxic, quadrupally charged anion was not absorbed; it could therefore be used as an osmotically active solute with reflection coefficient of 1.0 to adjust rates of fluid absorption, Jv, and to measure the coefficient of osmotic flow, Lp. The clearances from the perfusion fluid of all other test solutes were approximately proportional to Jv. From Lp and rates of clearances as a function of Jv and molecular size we estimate (a) the fraction of fluid absorption which passes paracellularly (approx. 50%), (b) coefficients of solvent drag of various solutes within intercellular junctions, (c) the equivalent pore radius of intercellular junctions (50 A) and their cross sectional area per unit path length (4.3 cm per cm length of intestine). Glucose absorption also varied as a function of Jv. From this relationship and the clearances of inert markers we calculate the rate of active transport of glucose, the amount of glucose carried paracellularly by solvent drag or back-diffusion at any given Jv and luminal glucose concentration and the concentration of glucose in the absorbate. The results indicate that solvent drag through paracellular channels is the principal route for intestinal transport of glucose or amino acids at physiological rates of fluid absorption and concentration. In the absence of luminal glucose the rate of fluid absorption and the clearances of all inert hydrophilic solutes were greatly reduced. It is proposed that Na-coupled transport of organic solutes from lumen to intercellular spaces provides the principal osmotic force for fluid absorption and triggers widening of intercellular junctions, thus promoting bulk absorption of nutrients by solvent drag. Further evidence for regulation of channel width is provided in accompanying papers on changes in electrical impedance and ultrastructure of junctions during Na-coupled solute transport.

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GALACTOSE TRANSPORT ACROSS RAT SMALL INTESTINE IN VIVO FOLLOWING DISTAL RESECTIONS OF VARYING EXTENTS

Cited by 8 publications

References 25 publications

Does apical membrane GLUT2 have a role in intestinal glucose uptake?

Does apical membrane GLUT2 have a role in intestinal glucose uptake?

Comparative effect of distal and proximal intestinal resection and bypass on the rat exocrine pancreas

Contribution of solvent drag through intercellular junctions to absorption of nutrients by the small intestine of the rat

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