scholarly journals α-Aminoisobutyric Acid Transport in the Midgut of Two Lepidopteran Larvae

1984 ◽  
Vol 108 (1) ◽  
pp. 329-339
Author(s):  
V. F. SACCHI ◽  
G. M. HANOZET ◽  
B. GIORDANA
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Intracellular Accumulation ◽  
Aminoisobutyric Acid ◽  
Lepidopteran Larvae ◽  
The Relationship ◽  
Columnar Cells ◽  
Low K

1. A net absorption of α-aminoisobutyric acid (AIB) takes place in vitro in the midgut of two lepidopteran larvae, Philosamia cynthia Drury and Bombyx mori L. 2. InP. cynthia the midgut epithelium accumulates AIB from the lumen, while in the same conditions AIB accumulation is not observed in B. mori midgut cells. 3. In P. cynthia, when the lumen is bathed with a low K solution, the net absorption of AIB is reduced and the intracellular accumulation from the lumen is abolished. 4. Brush border membrane vesicles, prepared from the midgut of both species, show a transient K-dependent concentrative uptake of AIB. 5. The relationship between AIB uptake and AIB concentration in the presence of a transmembrane K gradient was studied in B. mori vesicles and the kinetic constants were calculated. 6. These results confirm that there is a K-amino acid co-transport system on the brush border of columnar cells in the midgut of both larvae.

Cholera toxin facilitates calcium transport in jejunal brush border vesicles

1986 ◽  
Vol 64 (5) ◽  
pp. 568-574 ◽  
Author(s):  
David D. Maenz ◽  
G. W. Forsyth
Keyword(s):  
Cholera Toxin ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Equilibrium Dialysis ◽  
Membrane Vesicles ◽  
Second Messenger ◽  
Brush Border Membrane Vesicles ◽  
Ionophore A23187

Cholera toxin is very well characterized in terms of the activation of adenylate cyclase. In some systems, however, this cyclase activation does not seem to account for all of the physiological responses to the toxin. On the premise that cholera toxin may also exert effects through other second messenger compounds we have studied the effect of cholera toxin on the rate of Ca2+ movement across the membrane of intestinal brush border vesicles. Increasing concentrations of cholera toxin progressively accelerated the passive uptake of Ca2+ into, and the efflux of Ca2+ from, an osmotically active space in brush border membrane vesicles. This effect of cholera toxin was saturable by excess Ca2+ and was relatively specific, as the toxin did not affect vesicle permeability to an uncharged polar solute. The toxin had two high affinity Ca2+ binding sites on the A subunit as measured by equilibrium dialysis. Ca2+ transport facilitated by cholera toxin was temperature dependent, required the holotoxin, and could be inhibited by preincubation of the toxin with excess free ganglioside GM1.This increased rate of Ca2+ influx caused by the in vitro addition of cholera toxin to brush border membrane vesicles may have physiological significance as it was comparable to rates observed with the Ca ionophore A23187. Similar effects occurring in vivo could permit cholera toxin to increase cytoplasmic Ca2+ concentrations and to produce accompanying second messenger effects.

Lipid peroxidation of the brush-border membrane: membrane physical properties and glucose transport

1993 ◽  
Vol 264 (6) ◽  
pp. G1009-G1015 ◽  
Author(s):  
D. Jourd'Heuil ◽  
P. Vaananen ◽  
J. B. Meddings
Keyword(s):  
Lipid Peroxidation ◽  
Physical Properties ◽  
Glucose Transport ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Membrane Lipid ◽  
Membrane Function ◽  
Membrane Lipid Bilayer

During inflammatory conditions, peroxidation of biological membranes often takes place. Deleterious physiological consequences, in terms of membrane function, could theoretically be mediated by either direct oxidative attack upon integral membrane proteins or by indirectly altering the lipid environment surrounding these proteins. To address this issue, in vitro peroxidation of guinea pig brush-border membrane vesicles was induced by incubation of the vesicles with ferrous sulfate and ascorbic acid. We found that ongoing peroxidative attack initiates lipid peroxidation and radically alters the physical properties of the membrane lipid bilayer in a well-defined and regional manner. Peroxidation of microvillous membrane produced an increasingly rigid membrane. Coupled with these alterations was a fivefold reduction in maximal rates of sodium-dependent glucose transport that appeared to have a multifactorial origin. Approximately one-third of this reduction was secondary to altered membrane physical properties and was reversible by fluidizing the vesicles and returning membrane physical properties to normal. The remaining reduction in glucose transport activity was not responsive to membrane fluidization and was presumably related to direct damage of the transport protein.

Effect of Na+ on intestinal succinate transport and metabolism in vitro

1988 ◽  
Vol 255 (1) ◽  
pp. C95-C101 ◽  
Author(s):  
A. J. Moe ◽  
R. T. Mallet ◽  
M. J. Jackson ◽  
J. A. Hollywood ◽  
J. K. Kelleher
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Tricarboxylic Acid Cycle ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Co2 Production ◽  
Intestinal Brush Border Membrane ◽  
14Co2 Production ◽  
Rat Enterocytes

The effect of Na+ on 14CO2 production from [14C]succinate was studied in isolated rat enterocytes, and Na+-dependent succinate transport was characterized in pig intestinal brush-border membrane vesicles. The production of 14CO2 from [14C]succinate by enterocytes was decreased 12-fold when Na+ was replaced by N-methyl-D-glucamine in the absence of glutamine and 20-fold in the presence of 0.2 or 0.5 mM glutamine. The ratio of 14CO2 produced from [1,4-14C]succinate to that produced by [2,3-14C]succinate was not affected by Na+ replacement, indicating that the pattern of tricarboxylic acid cycle metabolism was not altered. The uptake of [14C]succinate by brush-border membrane vesicles was stimulated 10-fold in the presence of 100 mM NaCl compared with 100 mM KCl. When succinate uptake was corrected to transport into an osmotically sensitive space, the magnitude of the Na+ stimulation was 20-fold. Succinate transport into brush-border membrane vesicles was Na+ dependent, electroneutral, nonconcentrative, with an apparent Na+-succinate coupling ratio of 2:1. Results of this study indicate that Na+-stimulated CO2 production by enterocytes can be explained by the effect of Na+ on succinate transport across the brush-border membrane.

scholarly journals The effects of dietary ligands on zinc uptake at the porcine intestinal brush-border membrane

1990 ◽  
Vol 64 (3) ◽  
pp. 733-741 ◽  
Author(s):  
A. J. Turnbull ◽  
P. Blakeborough ◽  
R. P. H. Thompson
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Intestinal Brush Border Membrane ◽  
Intestinal Brush Border ◽  
Zn Uptake ◽  
Zn Concentration ◽  
Vitro Model

Intestinal brush-border-membrane vesicles were prepared from the porcine small bowel by magnesium precipitation and differential centrifugation, and were functionally intact. The influence of dietary ligands on 65Zn uptake was determined using a 65Zn concentration of 5 μm, an incubation time of 1 min and a reaction temperature of 27°, with a rapid filtration technique. At this low Zn concentration the addition of an excess of folate, histidine or glucose had no effect on Zn uptake. Addition of picolinate, citrate and phytate to the incubation medium significantly reduced Zn uptake at all concentrations of ligand examined. Any inhibitory effects of folic acid in vivo may thuss be due to a mucosal rather than lumen interaction. Those ligands inhibiting absorption may have done so through the formation of Zn-ligand complexes, which are either insoluble, or which reduce the binding of Zn to its mucosal receptor. This in vitro model of Zn absorption is useful for comparing the effects of potential Zn-binding ligands in the diet.

myo-Inositol transport in renal brush border vesicles and it inhibition by D-glucose

1980 ◽  
Vol 239 (2) ◽  
pp. F113-F120 ◽  
Author(s):  
M. R. Hammerman ◽  
B. Sacktor ◽  
W. H. Daughaday
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Initial Rate ◽  
Membrane Vesicles ◽  
Electrochemical Gradient ◽  
Patients With Diabetes ◽  
Dependent Transport ◽  
The Relationship ◽  
Inositol Uptake ◽  
Renal Brush Border

We examined the mechanism of myo-inositol uptake by rabbit renal proximal tubule brush border membrane vesicles and characterized the relationship between the transports of myo-inositol and D-glucose. A 100 mM Na+ electrochemical gradient (extravesicular medium > intravesicular medium) stimulated the initial rate of myo-inositol uptake 20- to 60-fold. Other cation gradients were ineffective. The Na+ myo-inositol co-transport system was shown to be electrogenic. The Na+ electrochemical gradient-dependent uptake of myo-inositol saturated at about 1 mM myo-inositol, with an apparent Km of 94 micro M at an initial 100 mM Na+ gradient. D-Glucose was an inhibitor of the Na+ gradient-dependent uptake of myo-inositol. D-Glucose, but not L-glucose, elicited accelerative exchange diffusion of myo-inositol. myo-Inositol did not significantly inhibit the Na+ gradient-dependent transport of D-glucose. We suggest that D-glucose inhibits myo-inositol uptake by dissipating the membrane potential and sharing the myo-inositol carrier. The inhibition of myo-inositol transport across the brush border membrane by D-glucose explains how glycosuria could produce inosituria in patients with diabetes mellitus.

Ontogeny of DA1 receptor-mediated natriuresis in the rat: in vivo and in vitro correlations

1992 ◽  
Vol 263 (3) ◽  
pp. R631-R638 ◽  
Author(s):  
S. Kaneko ◽  
F. Albrecht ◽  
L. D. Asico ◽  
G. M. Eisner ◽  
J. E. Robillard ◽  
...  
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Receptor Subtypes ◽  
Renal Brush Border Membrane ◽  
Natriuretic Effect ◽  
Old Rats ◽  
22Na Uptake

The natriuretic and diuretic effects of dopamine are attenuated in the young. Because dopamine has actions on receptors (e.g., adrenergic, serotonin) other than dopamine, we studied a novel dopamine agonist, pramipexole, which has a selectivity to both DA1 and DA2-receptor subtypes. Intravenous administration of pramipexole resulted in a dose-related (1, 10, and 100 micrograms.kg-1.min-1) increase in urine flow and absolute and fractional sodium excretion and a decrease in mean arterial pressure (MAP) in three groups of rats studied. Pramipexole induced a greater decrease in MAP in 6- to 7- (n = 5) and 9- to 16- (n = 6) than in 3- to 4-wk-old (n = 8) rats; the natriuresis and diuresis were greatest in 12- to 16- and least in 3- to 4-wk-old rats. The renal effects of pramipexole were mainly due to actions at the DA1 receptor, since these effects were completely blocked by the coinfusion of a DA1 antagonist, SKF 83742. To explore further a cause of the attenuated natriuretic effect of pramipexole in the young, we studied the effect of a selective DA1-receptor agonist, fenoldopam, on amiloride-sensitive 22Na+ uptake in renal brush-border membrane vesicles. The 3-s amiloride-sensitive uptake was inhibited (45%) by fenoldopam (5 x 10(-5)M) in 9- to 16- (n = 6) but not in 3- to 4-wk-old (n = 5) rats. These studies suggest that the attenuated natriuretic effect of dopamine in the young is in part due to decreased DA1 action on the brush-border membrane Na(+)-H+ exchanger.

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