Isoosmotic Transport of Fluid Across the Hamster Small Intestine in the Presence of Phlorizin-Induced Inhibition of Sugar Transport

1975 ◽  
Vol 53 (3) ◽  
pp. 375-382
Author(s):  
P. K. Dinda ◽  
Marjorie Beck ◽  
Ivan T. Beck
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Active Transport ◽  
Sodium Transport ◽  
Glucose Concentration ◽  
Sugar Transport ◽  
Potential Difference ◽  
Inherent Property ◽  
Osmoregulatory Mechanism ◽  
Neutral Sodium

Experiments were performed to investigate whether the fluid transported across the small intestine is isoosmotic with the mucosal solution when the active transport of glucose is partially inhibited. Everted hamster mid small intestine was incubated in one of the following four mucosal solutions: (1) Isotonic control, Krebs–Ringer bicarbonate solution containing 10 mM glucose (KRBSG); (2) Isotonic with phlorizin, KRBSG + 5 × 10−5 M phlorizin; (3) Hypertonic control, KRBSG + 50 mM mannitol; (4) Hypertonic with phlorizin, KRBSG + 50 mM mannitol + 5 × 10−5 M phlorizin. The serosal surface of the intestine was not bathed. Results indicate that the transported fluid was always isoosmotic with any of the mucosal solutions used. When the mucosal solution was made hypertonic with mannitol, the concentration of glucose and electrolytes in the absorbate increased, and as a result, the absorbate became hypertonic and isoosmotic with the mucosal solution. The presence of phlorizin either in the isotonic or in the hypertonic mucosal solution decreased the glucose concentration of the absorbate, but the transported fluid became isoosmotic with the mucosal solution due to a higher concentration of Na, K, and their associated anions. Phlorizin caused a decrease in the transmural potential difference. In spite of this, the presence of this glucoside in the mucosal solution increased the transport of sodium in relation to glucose transport. It is suggested that, at the concentrations used, phlorizin inhibits sodium movement through the electrogenic pathway, but increases the transport of this ion through the non-electrogenic route. This increase in neutral sodium transport seems to compensate for the low concentration of glucose in the absorbate, so that the absorbate becomes isoosmotic with the mucosal solution whether the latter is isotonic or hypertonic. It is suggested further that isoosmotic transport of fluid is an inherent property of the small intestine and that there may be an osmoregulatory mechanism in the gut which controls this process.

EFFECTS OF METABOLIC INHIBITORS ON POTASSIUM-STIMULATED GLUCOSE ABSORPTION BY ISOLATED SURVIVING GUINEA PIG INTESTINE

1958 ◽  
Vol 36 (3) ◽  
pp. 363-371 ◽  
Author(s):  
E. Riklis ◽  
J. H. Quastel
Keyword(s):  
Guinea Pig ◽  
Glucose Transport ◽  
Active Transport ◽  
Sugar Transport ◽  
Glucose Absorption ◽  
Metabolic Inhibitors ◽  
Enzymatic Mechanism ◽  
Potassium Stimulation ◽  
Low Concentrations ◽  
Stimulation Of

2,4-Dinitrophenol, at low concentrations, inhibits potassium-stimulated active transport of glucose by the isolated surviving guinea pig intestine to a greater extent than the unstimulated glucose transport. The potassium stimulation is abolished in the presence of 0.04 mM 2,4-dinitrophenol. Potassium stimulation of the active transport of glucose and galactose in the isolated guinea pig intestine is inhibited by phlorizin at low concentrations (0.01 mM) which have little or no effect on the unstimulated sugar transport. The presence of phlorizin has little or no effect on active fructose absorption, as shown by the combined transport of fructose and glucose derived from the fructose. In the presence of 15.6 meq./liter K+phlorizin exerts a small depression of the active transport of fructose. Potassium stimulation of the active transport of glucose in the isolated guinea pig intestine is inhibited by the narcotic luminal at low concentrations (2 mM). Luminal (10 mM) abolishes the potassium stimulation. Sodium malonate, at the concentration 2 mM, which exerts no inhibition of active glucose transport in isolated surviving guinea pig intestine, brings about over 40% inhibition of glucose transport when this is stimulated by potassium ions. Choline, at 0.5 mM, suppresses potassium stimulation of the active glucose transport in the isolated surviving guinea pig intestine. It is suggested that an enzymatic mechanism exists, associated with intestinal membranes, that controls sugar transport and that phosphorylations, either directly or indirectly, are connected with it.

EFFECTS OF METABOLIC INHIBITORS ON POTASSIUM-STIMULATED GLUCOSE ABSORPTION BY ISOLATED SURVIVING GUINEA PIG INTESTINE

1958 ◽  
Vol 36 (1) ◽  
pp. 363-371
Author(s):  
E. Riklis ◽  
J. H. Quastel
Keyword(s):  
Guinea Pig ◽  
Glucose Transport ◽  
Active Transport ◽  
Sugar Transport ◽  
Glucose Absorption ◽  
Metabolic Inhibitors ◽  
Enzymatic Mechanism ◽  
Potassium Stimulation ◽  
Low Concentrations ◽  
Stimulation Of

2,4-Dinitrophenol, at low concentrations, inhibits potassium-stimulated active transport of glucose by the isolated surviving guinea pig intestine to a greater extent than the unstimulated glucose transport. The potassium stimulation is abolished in the presence of 0.04 mM 2,4-dinitrophenol. Potassium stimulation of the active transport of glucose and galactose in the isolated guinea pig intestine is inhibited by phlorizin at low concentrations (0.01 mM) which have little or no effect on the unstimulated sugar transport. The presence of phlorizin has little or no effect on active fructose absorption, as shown by the combined transport of fructose and glucose derived from the fructose. In the presence of 15.6 meq./liter K+phlorizin exerts a small depression of the active transport of fructose. Potassium stimulation of the active transport of glucose in the isolated guinea pig intestine is inhibited by the narcotic luminal at low concentrations (2 mM). Luminal (10 mM) abolishes the potassium stimulation. Sodium malonate, at the concentration 2 mM, which exerts no inhibition of active glucose transport in isolated surviving guinea pig intestine, brings about over 40% inhibition of glucose transport when this is stimulated by potassium ions. Choline, at 0.5 mM, suppresses potassium stimulation of the active glucose transport in the isolated surviving guinea pig intestine. It is suggested that an enzymatic mechanism exists, associated with intestinal membranes, that controls sugar transport and that phosphorylations, either directly or indirectly, are connected with it.

The Potential Difference Across the Rectal Mucosa During Depressive Illness and Lithium Therapy

1975 ◽  
Vol 127 (2) ◽  
pp. 144-148 ◽  
Author(s):  
Malcolm Peet
Keyword(s):  
Active Transport ◽  
Sodium Transport ◽  
Rectal Mucosa ◽  
Lithium Carbonate ◽  
Depressive Illness ◽  
Potential Difference ◽  
Prophylactic Agent ◽  
Control Subjects ◽  
Manic Depressive ◽  
Depressive Patients

SummaryThe potential difference across the rectal mucosa (rectal p.d.) is generated by the active transport of sodium across the mucosa, and it is sensitive to the action of aldosterone. The rectal p.d. values of depressive patients on no treatment, tested whilst depressed or after recovery, were found to be similar to those of control subjects, indicating that sodium transport across the rectal mucosa and the activity of aldosterone were normal in these patients. This contrasts with previous reports of abnormalities of sodium transport and of aldosterone levels in manic-depressive patients. Manic-depressive patients taking lithium carbonate as a prophylactic agent were found to have significantly elevated rectal p.d. values when normothymic. Patients who had become depressed whilst taking lithium, and in whom prophylaxis had therefore failed, were found to have normal rectal p.d. values. Lack of elevation of rectal p.d. in response to lithium administration may be a characteristic of patients who fail to respond to lithium prophylaxis.

Dietary and developmental regulation of intestinal sugar transport

2001 ◽  
Vol 360 (2) ◽  
pp. 265-276 ◽  
Author(s):  
Ronaldo P. FERRARIS
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Molecular Mechanisms ◽  
Glucose Transporter ◽  
De Novo ◽  
Sugar Transport ◽  
Transport Systems ◽  
Intestinal Lumen ◽  
Transport Activity ◽  
Cellular Mechanisms

The Na+-dependent glucose transporter SGLT1 and the facilitated fructose transporter GLUT5 absorb sugars from the intestinal lumen across the brush-border membrane into the cells. The activity of these transport systems is known to be regulated primarily by diet and development. The cloning of these transporters has led to a surge of studies on cellular mechanisms regulating intestinal sugar transport. However, the small intestine can be a difficult organ to study, because its cells are continuously differentiating along the villus, and because the function of absorptive cells depends on both their state of maturity and their location along the villus axis. In this review, I describe the typical patterns of regulation of transport activity by dietary carbohydrate, Na+ and fibre, how these patterns are influenced by circadian rhythms, and how they vary in different species and during development. I then describe the molecular mechanisms underlying these regulatory patterns. The expression of these transporters is tightly linked to the villus architecture; hence, I also review the regulatory processes occurring along the crypt-villus axis. Regulation of glucose transport by diet may involve increased transcription of SGLT1 mainly in crypt cells. As cells migrate to the villus, the mRNA is degraded, and transporter proteins are then inserted into the membrane, leading to increases in glucose transport about a day after an increase in carbohydrate levels. In the SGLT1 model, transport activity in villus cells cannot be modulated by diet. In contrast, GLUT5 regulation by the diet seems to involve de novo synthesis of GLUT5 mRNA synthesis and protein in cells lining the villus, leading to increases in fructose transport a few hours after consumption of diets containing fructose. In the GLUT5 model, transport activity can be reprogrammed in mature enterocytes lining the villus column. Innovative experimental approaches are needed to increase our understanding of sugar transport regulation in the small intestine. I close by suggesting specific areas of research that may yield important information about this interesting, but difficult, topic.

Oral vanadate reduces Na(+)-dependent glucose transport in rat small intestine

Diabetes ◽  
1993 ◽  
Vol 42 (8) ◽  
pp. 1126-1132 ◽  
Author(s):  
K. L. Madsen ◽  
V. M. Porter ◽  
R. N. Fedorak
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Rat Small Intestine

scholarly journals Evidence for two asymmetric conformational states in the human erythrocyte sugar-transport system

1975 ◽  
Vol 145 (3) ◽  
pp. 417-429 ◽  
Author(s):  
J E Barnett ◽  
G D Holman ◽  
R A Chalkley ◽  
K A Munday
Keyword(s):  
Glucose Transport ◽  
Transport System ◽  
Human Erythrocyte ◽  
Partition Coefficients ◽  
External Medium ◽  
Sugar Transport ◽  
Conformational States ◽  
Glucose Transport System ◽  
Oil Water

6-O-methyl-, 6-O-propyl-, 6-O-pentyl- and 6-O-benzyl-D-galactose, and 6-O-methyl-, 6-O-propyl- and 6-O-pentyl-D-glucose inhibit the glucose-transport system of the human erythrocyte when added to the external medium. Penetration of 6-O-methyl-D-galactose is inhibited by D-glucose, suggesting that it is transported by the glucose-transport system, but the longer-chain 6-O-alkyl-D-galactoses penetrate by a slower D-glucose-insensitive route at rates proportional to their olive oil/water partition coefficients. 6-O-n-Propyl-D-glucose and 6-O-n-propyl-D-galactose do not significantly inhibit L-sorbose entry or D-glucose exit when present only on the inside of the cells whereas propyl-beta-D-glucopyranoside, which also penetrates the membrane slowly by a glucose-insensitive route, only inhibits L-sorbose entry or D-glucose exit when present inside the cells, and not when on the outside. The 6-O-alkyl-D-galactoses, like the other nontransported C-4 and C-6 derivatives, maltose and 4,6-O-ethylidene-D-glucose, protect against fluorodinitrobenzene inactivation, whereas propyl beta-D-glucopyranoside stimulates the inactivation. Of the transported sugars tested, those modified at C-1, C-2 and C-3 enhance fluorodinitrobenzene inactivation, where those modified at C-4 and C-6 do not, but are inert or protect against inactivation. An asymmetric mechanism is proposed with two conformational states in which the sugar binds to the transport system so that C-4 and C-6 are in contact with the solvent on the outside and C-1 is in contact with the solvent on the inside of the cell. It is suggested that fluorodinitrobenzene reacts with the form of the transport system that binds sugars at the inner side of the membrane. An Appendix describes the theoretical basis of the experimental methods used for the determination of kinetic constants for non-permeating inhibitors.

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