scholarly journals Oleic acid uptake into rat and rabbit jejunal brush border membrane

1995 ◽  
Vol 1236 (1) ◽  
pp. 51-64 ◽  
Author(s):  
C Schoeller ◽  
M Keelan ◽  
G Mulvey ◽  
W Stremmel ◽  
A.B.R Thomson
1981 ◽  
Vol 240 (3) ◽  
pp. F185-F191 ◽  
Author(s):  
E. F. Boumendil-Podevin ◽  
R. A. Podevin

The transport of nicotinic acid was investigated in brush border membrane vesicles isolated from rabbit kidney. The imposition of a Na+ gradient (out to in) induced a transient stimulation of nicotinic acid uptake above its final equilibrium value. This stimulation was specific for Na+. The uptake of nicotinic acid by the brush border membranes represented transport into an internal space and occurred in the absence of significant nicotinic acid degradation. The Na+ gradient-dependent uptake of nicotinic acid was saturable, apparent Km = 0.3 mM. Uptake of nicotinic acid was inhibited by its two isomers: picolinic and isonicotinic acid. In contrast, pyridine derivatives with two carboxyl groups or an amide group in addition to the carboxyl group were without inhibitory effect. Evaluation of changes in membrane potential using the lipophilic cation triphenylmethylphosphonium demonstrated that conditions that transiently generated either an interior-positive or an interior-negative membrane potential failed to affect the Na+-dependent transport of nicotinic acid. These findings provide evidence of the existence on the luminal membrane of a Na+ gradient-dependent and electroneutral transport system for nicotinic acid.


1986 ◽  
Vol 251 (2) ◽  
pp. G218-G222 ◽  
Author(s):  
J. Zimmerman ◽  
J. Selhub ◽  
I. H. Rosenberg

The effect of sodium on folate transport across the intestinal luminal membrane was analyzed using two techniques: the "influx" chamber and isolated brush-border membrane vesicles. Preincubation of tissue in Na+-free medium did not have a consistent effect on folic acid influx provided that Na+ was present in the test solution. Replacement of Na+ in the test solution by choline+ resulted in a significant reduction of folic acid influx. However, when intestinal sheets that had been equilibrated in Na+-free solution were exposed to test solution containing either Na+, Li+, K+, Rb+, Cs+, Tris+, or guanidinium+ as main cations, folic acid influx was not significantly decreased. Concentration-dependence studies showed that replacement of Na+ by Rb+ did not affect the saturable mechanism of folate transport. Rather, a decrease in nonsaturable folic acid uptake accounted for the slightly reduced influx observed in the presence of Rb+. Experiments with brush-border membrane vesicles revealed that methotrexate uptake was significantly higher in the presence of external Na+ than in the presence of K+, but was not different from uptake in the presence of K+ plus valinomycin. These data suggest that the saturable component of folate transport is not Na+ dependent, and nonsaturable transport of folic acid across the luminal membrane occurs in part through a conductive pathway that involves a negatively charged species of folate and a cation whose membrane permeability affects the rate of folate transport. The importance of Na+ in this process in vivo derives from the fact that Na+ is the most permeant cation available at the absorptive site in the small intestine.


1987 ◽  
Vol 252 (1) ◽  
pp. G33-G39 ◽  
Author(s):  
V. M. Rajendran ◽  
J. M. Harig ◽  
M. B. Adams ◽  
K. Ramaswamy

This study characterizes the transport of radiolabeled acidic amino acids into brush-border membrane vesicles prepared from human jejunum. The uptakes of L-glutamic, L-aspartic, and D-aspartic acids were stimulated by a Na+ gradient (extravesicular greater than intravesicular). Concentrative uptake (resulting in an "overshoot" phenomenon) of these dicarboxylic amino acids occurred when there was an outward K+ gradient (intravesicular greater than extravesicular). In addition, increasing K+ gradients (0-100 mM) resulted in enhanced uptake of L-glutamic acid. This K+ requirement is somewhat specific as Rb+ and Cs+ could enhance uptake to a limited extent, whereas Li+ and choline+ showed no enhancement. The presence of a K+ gradient did not affect the affinity of the carrier system for L-glutamic acid but it did increase the Vmax. The presence of extravesicular anions having differing membrane permeabilities did not alter L-glutamic acid uptake indicating an absence of an effect of membrane potential on the transport process. Finally, the human transport system for L-glutamic acid appears to be specific for acidic amino acids as demonstrated by inhibition studies. Our studies demonstrate a transport system in human jejunum specific for acidic amino acids that is energized by an inward Na+ gradient and an outward K+ gradient.


1987 ◽  
Vol 252 (5) ◽  
pp. G614-G625 ◽  
Author(s):  
W. H. Karasov ◽  
D. H. Solberg ◽  
J. M. Diamond

To understand how intestinal amino acid (AA) transport is regulated by dietary substrate levels, we measured uptake of seven AAs and glucose across the jejunal brush-border membrane of mice kept on one of three isocaloric rations differing in nitrogen content. In the high-protein ration, uptake increased by 77-81% for the nonessential, less toxic AAs, proline, and aspartate but only by 32-61% for the more toxic essential AAs tested. In the nitrogen-deficient ration, uptake decreased for the nonessential aspartate and proline but stayed constant or increased for essential AAs and for the nonessential alanine. These patterns imply independent regulation of the intestine's various AA transporters. With decreasing dietary AA (or protein), the imino acid and acidic AA "private" transporters are repressed, while activities of the basic AA transporter and the neutral AA "public" transporter decrease to an asymptote or else go through a minimum. These regulatory patterns can be understood as a compromise among conflicting constraints imposed by protein's multiple roles as a source of calories, nitrogen, and essential AAs and by the toxicity of essential AAs at high concentrations.


1985 ◽  
Vol 63 (4) ◽  
pp. 249-256 ◽  
Author(s):  
P. Proulx ◽  
H. Aubry ◽  
I. Brglez ◽  
D. G. Williamson

Initial studies revealed that the uptake of palmitic acid and oleic acid into brush border membranes was similar when these were isolated from either whole small intestine, jejunum, or ileum. The uptake of these fatty acids was somewhat lower with membranes obtained from duodenum. Subsequent studies, all with membranes obtained from whole intestine, indicated an increase in binding with chain length of fatty acid of up to 16 carbons. Unsaturation decreased this uptake somewhat. Taurocholate and 1-palmitoyl lysolecithin had a moderate stimulatory effect on the binding of oleic acid and palmitic acid at concentrations of 10 and 0.5 mM, respectively, and inhibited at higher concentrations. Addition of 1.4 mM egg lecithin to the fatty acid – bile salt micelles, such that the lecithin – bile salt ratio was 0.2, decreased the uptake of fatty acids generally, but did not significantly affect the pattern of binding by membrane fractions isolated from different segments nor did it change the pattern of labelling when fatty acid chain length and unsaturation were varied. At lower concentrations, egg lecithin had little effect on the uptake of oleic acid, whereas dipalmitoyl phosphatidylcholine stimulated binding of both palmitic acid and oleic acid over the entire range of concentrations tested. Preincubation of the membranes with this saturated phospholipid stimulated the uptake of oleic acid, and addition of this choline lipid to the oleic acid – bile salt containing micelles did not substantially enhance fatty acid uptake in lipid-treated membranes. The binding of fatty acid was very rapid either in the presence or the absence of Ca2+, such that even in zero-time controls essentially equilibrium bindings were obtained. The presence of Ca2+ stimulated the incorporation substantially. The results as a whole indicate that fatty acid uptake into brush border membrane is very responsive to a variety of conditions which could prevail in the gut during the absorption process.


1981 ◽  
Vol 241 (2) ◽  
pp. G83-G92 ◽  
Author(s):  
F. A. Wilson

The intestinal absorption of bile acids is determined by two resistances: diffusion through an unstirred water layer and penetration of the cell membrane. Passive jejunal uptake of polar bile acids is limited by the mucosal membrane, whereas the unstirred layer exerts resistance on uptake of more nonpolar species. After correction for the diffusion layer, the membrane permeability coefficients were derived to calculate the delta delta Fw leads to 1 associated with uptake of the -OH (+874 cal.mol-1), glycine (+897), and taurine (+1,498) groups. The delta delta F1 (-6,126 cal.mol-1) for the -OH group suggested that the jejunal mucosa is a relatively polar membrane. The unstirred layer is even more rate limiting for bile acid uptake from micellar solutions. Once the micelle reaches the aqueous-membrane interface, it is not absorbed intact, but rather uptake is explained in terms of monomers in the aqueous phase that are in equilibrium with the micelle. The presence of the unstirred water layer introduces artifactually high Km values for active transport. Structure-activity studies suggest that the ileal recognition site consists of a component for the steroid moiety, a positive charge, and an adjacent anionic charge. The energy for active transport arises from the Na+ gradient across the brush-border membrane that, in turn, is dependent on the activity of Na+-K+-ATPase. The Na+ stimulation of bile acid transport across the ileal brush-border membrane is due to influx coupling via a cotransport system rather than electrical coupling to satisfy overall electrical neutrality.


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