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Chris I. Cheeseman - One of the best experts on this subject based on the ideXlab platform.

  • the effect of gip and glucagon like peptides on intestinal Basolateral Membrane hexose transport
    American Journal of Physiology-gastrointestinal and Liver Physiology, 1996
    Co-Authors: Chris I. Cheeseman, R Tsang
    Abstract:

    The effect of gastric inhibitory polypeptide (GIP) and the related glucagon-like peptides-1 and -2 (GLP-1 and GLP-2) on jejunal Basolateral Membrane glucose transport was investigated to determine if the upregulation produced by luminal hexoses could be explained by the release of one or more of these peptides. Luminal perfusion of the rat jejunum for 4 h, under pentobarbital sodium anesthesia, with 100 mM D-glucose produced a significant increase in plasma GIP levels. Vascular infusion of saline containing 100-800 pM GIP also increased the maximal transport rate for carrier-mediated glucose uptake in jejunal Basolateral Membrane vesicles. The effect of vascular 400 pM GIP was maximal after 1 h and maintained out to 4 h. The effect of luminal glucose could be blocked by preinjection with anti-GIP antibodies, whereas an antineurotensin antibody had no effect. Vascular infusion with 800 pM GLP-1-(7-36) amide had no effect, but GLP-2 (400 and 800 pM) increased the D-glucose maximal transport rate. An anti-GLP antibody was able to block the response to luminal glucose.

  • Evidence for a lactate-anion exchanger in the rat jejunal Basolateral Membrane
    Gastroenterology, 1994
    Co-Authors: Chris I. Cheeseman, Salima Shariff, Debbie O'neill
    Abstract:

    Abstract Background/Aims: The mechanism by which lactate, absorbed from the intestinal lumen or generated within the epithelium, crosses the Basolateral Membrane of the enterocyte and enters the bloodstream has not previously been characterized in detail. Methods: l-lactate uptake into and efflux from isolated jejunal Basolateral Membrane vesicles was investigated at room temperature using rapid filtration techniques. Results: Furosemide sensitive uptake of l-lactate was unaffected by cis sodium or proton gradients but could be stimulated by a trans gradient of bicarbonate and chloride. Kinetic analysis showed uptake to consist of a saturable component with a Michaelis constant ( K m ) of 3.2 mmol/L and a maximum velocity (V max ) of 67 pmol·mg protein −1 · s −1 and a nonsaturable α-4-hydroxy-cinnamic acid insensitive component. Pyruvate, butyrate, acetate, valerate, and proprionate competitively inhibited lactate uptake into the vesicles. Efflux of lactate from preloaded vesicles was furosemide sensitive and accelerated by a trans bicarbonate gradient as well as by 10 mmol/L acetate, butyrate, and pyruvate. Conclusions: It is concluded that there is a short chain-fatty acid carrier system in the intestinal Basolateral Membrane, which operates as an anion exchanger.

  • GLUT2 Is the Transporter Basolateral Membrane
    1993
    Co-Authors: Chris I. Cheeseman
    Abstract:

    Back.@ound: The exact roles of disaccharidases and GLUT5 in the brush border Membrane and GLUT2 in the Basolateral Membrane in the absorption of fructose across the intestine have not been fully determined. This paper describes characterization of fructose transport across the jejunal Basolateral Membrane using isolated Membrane vesicles. Methods: Transport of fructose was measured using rapid filtration of vesicles. Luminal perfusion in vivo with glucose and fructose before vesicle preparation was used to assess modulation of GLUT2 activity. Western blotting measured the abundance of GLUT2 in the Membrane. Results: The maximal rate of transport for fructose was 1100 pmol/mg protein/s and the Michaelis constant was 16 mmol/L. Fructose and glucose could completely inhibit the transport of each other. Perfusion of the intestinal lumen with fructose or glucose saline for 4 hours produced a fourfold increase in maximal fructose transport. Conclusions: These data indicate that the one transport protein, GLUT2, is responsible for moving both fructose and glucose out of the enterocyte across the Basolateral Membrane under basal conditions. The activity of this, or a closely related carrier, is rapidly upregulated by the presence of hexoses in the intestinal lumen, explaining the potentiation of fructose absorption by luminal glucose and obviating any need to involve apical disaccharidases.

  • GLUT2 is the transporter for fructose across the rat intestinal Basolateral Membrane
    Gastroenterology, 1993
    Co-Authors: Chris I. Cheeseman
    Abstract:

    Abstract Background : The exact roles of disaccharidases and GLUT5 in the brush border Membrane and GLUT2 in the Basolateral Membrane in the absorption of fructose across the intestine have not been fully determined. This paper describes characterization of fructose transport across the jejunal Basolateral Membrane using isolated Membrane vesicles. Methods : Transport of fructose was measured using rapid filtration of vesicles. Luminal perfusion in vivo with glucose and fructose before vesicle preparation was used to assess modulation of GLUT2 activity. Western blotting measured the abundance of GLUT2 in the Membrane. Results : The maximal rate of transport for fructose was 1100 pmol/mg protein/s and the Michaelis constant was 16 mmol/L. Fructose and glucose could completely inhibit the transport of each other. Perfusion of the intestinal lumen with fructose or glucose saline for 4 hours produced a fourfold increase in maximal fructose transport. Conclusions : These data indicate that the one transport protein, GLUT2, is responsible for moving both fructose and glucose out of the enterocyte across the Basolateral Membrane under basal conditions. The activity of this, or a closely related carrier, is rapidly upregulated by the presence of hexoses in the intestinal lumen, explaining the potentiation of fructose absorption by luminal glucose and obviating any need to involve apical disaccharidases.

  • adaptation of glucose transport across rat enterocyte Basolateral Membrane in response to altered dietary carbohydrate intake
    The Journal of Physiology, 1991
    Co-Authors: Chris I. Cheeseman, B Harley
    Abstract:

    1. The effect of changes in the carbohydrate content of the diet on D-glucose transport across the Basolateral Membrane of rat enterocytes has been compared with alterations in transport across the brush-border Membrane. 2. Measurement of carrier-mediated D-glucose uptake across the jejunal brush border from animals fed a low- or high-carbohydrate diet showed a change in the maximal rate of transport by 7 days which was maintained for 14 days. The low-carbohydrate diet produced a progressive decline in uptake whereas the high-carbohydrate diet increased the transport. There was no alteration in the apparent affinity constant as a result of the dietary manipulations and no discernible trend for changes in the passive permeability to glucose. 3. Transport of D-glucose across the Basolateral Membrane was also affected by the dietary composition. After 7 days the maximal transport rate was greater in the animals fed the high-carbohydrate diet. However, while this increase was maintained for 14 days, uptake into vesicles prepared after 2 weeks on the low-carbohydrate diet showed a return to control levels. 4. A detailed analysis of the time course of these responses showed the effect on Basolateral Membrane transport to be inducible within 3 days of switching from the low- to the high-carbohydrate diet and could be reversed within a similar period. 5. Kinetic studies using purified Basolateral Membrane vesicles confirmed that the change in transport was the result of an increase in the maximal transport rate. Analysis of cytochalasin B binding to these Membranes showed a parallel change in the number of glucose-inhibitable binding sites. 6. The component of the diet responsible for these changes was further investigated by replacing the glucose in the high-carbohydrate food with galactose, fructose, mannose or 3-O-methylglucose. Only glucose and fructose produced any significant change in the transport across the Basolateral Membrane. 7. It is concluded that in response to changes in the carbohydrate content of the diet there are alterations in the capacity for glucose transport across the Basolateral Membrane of the enterocyte as well as in the brush-border Membrane. The change in transport across the Basolateral Membrane is best explained by an increase in the number of glucose carriers in this Membrane.

Sheldon S. Miller - One of the best experts on this subject based on the ideXlab platform.

Michael J. O'donnell - One of the best experts on this subject based on the ideXlab platform.

P. Ripoche - One of the best experts on this subject based on the ideXlab platform.

  • Evidence for permanent water channels in the Basolateral Membrane of an ADH-sensitive epithelium
    The Journal of Membrane Biology, 1991
    Co-Authors: F. Goot, B. Corman, P. Ripoche
    Abstract:

    The transepithelial water permeability in frog urinary bladder is believed to be essentially dependent on the ADH-regulated apical water permeability. To get a better understanding of the transmural water movement, the diffusional water permeability ( P _d) of the Basolateral Membrane of urinary bladder was studied. Access to this post-luminal barrier was made possible by “perforating” the apical Membrane with amphotericin B. The addition of this antibiotic increased P _d from 1.12±0.10×10^−4 cm/sec ( n =7) to 4.08±0.33×10^−4 cm/sec ( n =7). The effect of mercuric sulfhydryl reagents, which are commonly used to characterize water channels, was tested on amphotericin B-treated bladders. HgCl_2 (10^−3 m ) decreased P _d by 52% and para -chloromercuribenzoic acid ( p CMB) (1.4×10^−4 m ) by 34%. The activation energy for the diffusional water transport was found to increase from 4.52±0.23 kcal/mol ( n =3), in the control situation, to 9.99±0.91 kcal/mol ( n =4) in the presence of 1.4×10^−4 m p CMB. Our second approach was to measure the kinetics of water efflux, by stop-flow light scattering, on isolated epithelial cells from urinary bladders. p CMB (0.5 or 1.4×10^−4 m ) was found to inhibit water exit by 91±2%. These data strongly support the existence of proteins responsible for water transport across the Basolateral Membrane, which are permanently present.

P P Sokol - One of the best experts on this subject based on the ideXlab platform.

  • mechanism of vancomycin transport in the kidney studies in rabbit renal brush border and Basolateral Membrane vesicles
    Journal of Pharmacology and Experimental Therapeutics, 1991
    Co-Authors: P P Sokol
    Abstract:

    The effect of vancomycin, a putatively nephrotoxic amine glycopeptide antibiotic, on the transport of organic cations was examined in rabbit renal Basolateral and brush border Membrane vesicles. The studies were conducted using a rapid filtration technique and the prototypic organic cation tetraethylammonium. In Basolateral Membrane vesicles, vancomycin cis-inhibited the electrogenic transport of tetraethylammonium with an IC50 value of 260 microM. In contrast, gentamicin, an aminoglycoside, was without effect. Inhibition by mepiperphenidol, a classical organic cation transport inhibitor, was observed with an IC50 value of 24 microM. Countertransport, that is, trans-stimulation experiments, were initiated in order to determine whether or not vancomycin was capable of traversing the plasma Membrane. Vancomycin caused trans-stimulation of tetraethylammonium uptake. The specificity of inhibition was assessed by determining the effect of vancomycin on the transport of p-aminohippurate, an organic anion. Vancomycin did not inhibit transport, whereas probenecid, a classical organic anion inhibitor, did. In the brush border Membrane, vancomycin had no effect on the transport of tetraethylammonium. These data are consistent with mediated transport for vancomycin across the Basolateral Membrane, but not across the brush border Membrane. This implies that the nephrotoxicity of vancomycin may be due to entry through the Basolateral Membrane and the absence of mediated egress at the brush border Membrane.