Ionic effect on intestinal transport of glucose in the rat

1960 ◽  
Vol 198 (5) ◽  
pp. 1056-1058 ◽  
Author(s):  
T. Z. Csáky ◽  
Lawrence Zollicoffer
Keyword(s):  
Glucose Transport ◽  
Intestinal Transport ◽  
Glucose Absorption ◽  
Anesthetized Rats ◽  
Ionic Effect

A loop of upper jejunum of anesthetized rats was perfused in situ with glucose (500 mg/l.) dissolved in either isosmotic Na2SO4, Li2SO4, K2SO4 or MgSO4. Rapid glucose absorption takes place from the Na2SO4 solution, whereas the glucose transport is inhibited if Na is replaced. The rate of inhibition varied: 91% with Li, 86% with K and 75% with Mg. The inhibition is reversible by the subsequent perfusion of the same gut with Na2SO4.

Regulation of intestinal glucose transport

1992 ◽  
Vol 70 (9) ◽  
pp. 1201-1207 ◽  
Author(s):  
D. J. Philpott ◽  
J. D. Butzner ◽  
J. B. Meddings
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Intestinal Adaptation ◽  
Basolateral Membrane ◽  
Intestinal Transport ◽  
Glucose Absorption ◽  
Dietary Carbohydrate ◽  
Adaptive Responses ◽  
Carbohydrate Levels ◽  
Specific Regulation

The small intestine is capable of adapting nutrient transport in response to numerous stimuli. This review examines several possible mechanisms involved in intestinal adaptation. In some cases, the enhancement of transport is nonspecific, that is, the absorption of many nutrients is affected. Usually, increased transport capacity in these instances can be attributed to an increase in intestinal surface area. Alternatively, some conditions induce specific regulation at the level of the enterocyte that affects the transport of a particular nutrient. Since the absorption of glucose from the intestine is so well characterized, it serves as a useful model for this type of intestinal adaptation. Four potential sites for the specific regulation of glucose transport have been described, and each is implicated in different situations. First, mechanisms at the brush-border membrane of the enterocyte are believed to be involved in the upregulation of glucose transport that occurs in streptozotocin-induced diabetes mellitus and alterations in dietary carbohydrate levels. Also, factors that increase the sodium gradient across the enterocyte may increase the rate of glucose transport. It has been suggested that an increase in activity of the basolaterally located Na+–K+ ATPase could be responsible for this phenomena. The rapid increase in glucose uptake seen in hyperglycemia seems to be mediated by an increase in both the number and activity of glucose carriers located at the basolateral membrane. More recently, it was demonstrated that mechanisms at the basolateral membrane also play a role in the chronic increase in glucose transport observed when dietary carbohydrate levels are increased. Finally, alterations in tight-junction permeability enhance glucose absorption from the small intestine. The possible signals that prompt these adaptive responses in the small intestine include glucose itself and humoral as well as enteric nervous interactions.Key words: intestinal transport, glucose transport, intestinal adaptation.

scholarly journals Small Intestinal Glucose Transport

1967 ◽  
Vol 50 (5) ◽  
pp. 1173-1182 ◽  
Author(s):  
Alan K. Rider ◽  
Harold P. Schedl ◽  
George Nokes ◽  
Streeter Shining
Keyword(s):  
Glucose Transport ◽  
Absorption Rate ◽  
Distal Segment ◽  
Glucose Absorption ◽  
In Vivo Studies ◽  
Intestinal Segments ◽  
Small Intestinal ◽  
Rate Limiting

Proximal and distal small intestinal segments of the rat were perfused in situ at two different rates with isotonic solutions containing glucose in concentrations ranging from 25 to 600 mg/100 ml. Absorption was measured as glucose disappearance rate from the lumen. Glucose absorption had not previously been studied at intraluminal concentrations above and below blood glucose. Absorption was more rapid from the proximal segment. In both segments absorption was independent of perfusion rate and of whether glucose was analyzed by counting 14C or by the Somogyi method. The latter finding suggests that of the unidirectional fluxes, flux out of the bowel is much greater than flux into the bowel. In contrast to the findings in previous studies neither segment showed rate-limiting kinetics, and the Michaelis-Menten analysis was not applicable. The form of the curve depicting absorption rate in relation to concentration differed between the two segments. At the higher concentrations absorption rate continued to increase much more rapidly in the proximal than in the distal segment. The observations could not be explained by known mechanisms of glucose transport and illustrate the difficulties of achieving biochemically and physiologically meaningful in vivo studies of intestinal absorption.

Intestinal transport of HDND-7, a novel hesperetin derivative, in in vitro MDCK cell and in situ single-pass intestinal perfusion models

Xenobiotica ◽  
2016 ◽  
Vol 47 (8) ◽  
pp. 719-730 ◽  
Author(s):  
Ruonan Chen ◽  
Lan Li ◽  
Chenlin Shen ◽  
Cheng Huang ◽  
Taotao Ma ◽  
...  
Keyword(s):  
Mdck Cell ◽  
Intestinal Transport ◽  
Intestinal Perfusion ◽  
Single Pass

Alterations of band 3 transport protein by cellular aging and disease: erythrocyte band 3 and glucose transporter share a functional relationship

1990 ◽  
Vol 68 (12) ◽  
pp. 1419-1427 ◽  
Author(s):  
Gieljan J. C. G. M. Bosman ◽  
Marguerite M. B. Kay
Keyword(s):  
Glucose Transport ◽  
Structural Changes ◽  
Glucose Transporter ◽  
Functional Relationship ◽  
Band 3 ◽  
Anion Transport ◽  
Cellular Aging ◽  
Abnormal Band ◽  
Membrane Spanning

Structural changes in human erythrocyte band 3 that affect anion transport are correlated with changes in glucose transport in situ. Breakdown of band 3, observed during normal erythrocyte aging in situ and in some diseases involving erythrocytes, is associated with an increase in Km and a decrease in Vmax of sulfate self-exchange, and with an increase in Km and Vmax of glucose efflux. Erythrocytes containing a high molecular weight form of band 3 exhibit an increase in Vmax of sulfate exchange and a decrease in Vmax of glucose efflux. Identical transport characteristics are observed in abnormal band-3-containing erythrocytes from individuals with familial amyotrophic chorea with acanthocytosis. A third band 3 alteration, fast-aging band 3, exhibits decreased Vmax of sulfate exchange and an increase in Km and decrease in Vmax of glucose efflux. Changes in band 3 structure that are the result of unstable hemoglobin or a deficiency in glucose-6-phosphate dehydrogenase and that do not affect anion transport have no effect on glucose transport characteristics. These data indicate the existence of a functional relationship between the membrane-spanning, anion-transport domain of band 3 and glucose transport in human erythrocytes. Antibodies to synthetic peptides reveal structural changes in membranes from the three inborn band 3 alterations and in band 3 itself in membranes from fast-aging band 3. Thus, immunological data suggests a structural relationship between anion and glucose transporters.Key words: red cell, anion transport, membrane proteins, aging, choreoacanthocytosis, anemia.

EFFECTS OF CATIONS ON SUGAR ABSORPTION BY ISOLATED SURVIVING GUINEA PIG INTESTINE

1958 ◽  
Vol 36 (3) ◽  
pp. 347-362 ◽  
Author(s):  
E. Riklis ◽  
J. H. Quastel
Keyword(s):  
Guinea Pig ◽  
Glucose Transport ◽  
Active Transport ◽  
Glucose Absorption ◽  
Ion Concentration ◽  
Potassium Ions ◽  
Magnesium Ions ◽  
Sugar Absorption ◽  
Rate Of Absorption ◽  
High Concentrations

The rate of absorption of glucose from isolated surviving guinea pig intestine increases with increase of the concentration of glucose in the lumen until a maximum rate is obtained. The relation between absorption rate of glucose and initial glucose concentration conforms to an equation of the Michaelis–Menten type. The apparent Km(half saturation concentration) is 7 × 10−3M. Increase of the concentration of potassium ions in the Ringer–bicarbonate solution bathing the intestine leads to an increase of the rate of glucose absorption, this being most marked with 15.6 meq./liter K+and 14 mM glucose. No such stimulating action of potassium ions is observed on glucose absorption under anaerobic conditions. The effect of increased potassium ion concentration is to accelerate the rate of transport found with low concentrations of glucose to the maximum value found with high concentrations of the sugar. Sodium ions must be present for glucose absorption to take place and omission of magnesium ions from a Ringer–bicarbonate solution, containing 15.6 meq./liter K+, brings about a decreased rate of active glucose transport. Magnesium ions are necessary for the stimulated rate of glucose absorption obtained in the presence of potassium ions. The presence of ammonium ions decreases the rate of glucose absorption. Potassium ions may be effectively replaced by rubidium ions for stimulation of glucose transport. Cesium ions do not activate. The proportion of glucose to fructose appearing in the serosal solution, when fructose is absorbed from the mucosal solution, depends on the concentration of fructose present. The proportion may be as high as 9:1 with low (7 mM) fructose concentrations; it decreases with increasing fructose concentrations. The active transport of fructose, as demonstrated by the conversion of fructose in the isolated surviving guinea pig intestine, is enhanced by the presence of potassium ions (15.6 meq./liter). The rate of transport of fructose itself is unaffected by potassium. Using radioactive glucose and fructose, it is shown that the total amount of sugar transferred through the intestine as estimated by the radioactivity appearing in the serosal solution is approximately that calculated from chemical analyses. Potassium ions have no activating action on the transport of sugars such as sorbose, mannose, and D-glucosamine, but have a marked effect on galactose transport. The results support the conclusion that potassium ions do not influence active transport of glucose, fructose, and galactose by a change of intestinal permeability to these sugars, but do so by affecting a specific phase involved in the mechanism of active transport of sugars. The presence of L-glutamine stimulates active transport of glucose, whereas that of L-glutamate tends to diminish it.

Influence of vascular and luminal hexoses on rat intestinal basolateral glucose transport

1994 ◽  
Vol 72 (4) ◽  
pp. 317-326 ◽  
Author(s):  
Raymond Tsang ◽  
Ziliang Ao ◽  
Chris Cheeseman
Keyword(s):  
Glucose Transport ◽  
Plasma Glucose ◽  
Intestinal Adaptation ◽  
Basolateral Membrane ◽  
Physiological Role ◽  
Intestinal Transport ◽  
Membrane Vesicles ◽  
Luminal Perfusion

The influence of luminal and vascular hexoses in rats on glucose transport across the jejunal basolateral membrane (BLM) was measured using isolated membrane vesicles prepared from infused animals. In vivo vascular infusions of glucose produced an increase in glucose transport across BLM vesicles. Sucrose, mannose, galactose, and fructose had no significant effect. Plasma glucose concentrations were unaffected by galactose and sucrose vascular infusions, while mannose and fructose produced a modest rise, and glucose increased plasma glucose to 20 mM. Insulin release was significantly increased by vascular infusion of glucose and fructose, while mannose produced only a small sustained rise. Sucrose and galactose had no effect. Perfusion through the lumen of the rat jejunum in vivo, for up to 4 h, with glucose, fructose, sucrose, or lactate (100 or 25 mM) produced a significant increase in the maximal rate of glucose transport (up to 4- to 5-fold) across BLMs. Galactose and mannose had no effect. Luminal glucose perfusion produced a small nonsignificant increase in glucose inhibitable cytochalasin B binding to BLM vesicles, and no change was seen in the microsomal pool of binding sites. The abundance of GLUT2 in the jejunal BLM, as determined by Western blotting, was unaffected by luminal perfusion of 100 mM glucose for 4 h. Fructose almost completely inhibited the carrier-mediated uptake of glucose in control and upregulated jejunal BLM vesicles. These results are discussed in relation to the physiological role of the upregulation of GLUT2 activity by luminal and vascular hexoses.Key words: intestinal transport, basolateral membrane, glucose transport, intestinal adaptation.

scholarly journals The Effect of Potassium on the Intestinal Transport of Glucose

1966 ◽  
Vol 50 (1) ◽  
pp. 113-128 ◽  
Author(s):  
T. Z. Csáky ◽  
P. M. Ho
Keyword(s):  
Small Intestine ◽  
Specific Activity ◽  
Lactic Acid Production ◽  
Sugar Transport ◽  
Intestinal Transport ◽  
Intestinal Lumen ◽  
High K ◽  
Rate Of Absorption ◽  
Specific Sugar

The rate of absorption of glucose, galactose, and 3-0-methylglucose was studied in the rat's small intestine perfused in situ with isosmotic solutions containing these sugars and Na2SO4 or K2SO4. The presence of high [K+] in the lumen enhances absorption of glucose but not that of galactose or of 3-0-methylglucose. The potassium stimulation is apparent at higher glucose concentrations where primarily carrier-mediated diffusion is involved in the translocation. In this case potassium stimulates transport even if it is the only cation in the lumen. The potassium-stimulated intestine produces more glycogen with higher specific activity than the control gut. Lactic acid production by the intestine is markedly enhanced if the intestinal lumen is perfused with a solution containing glucose and high [K+]. It is concluded that potassium does not affect permeability or the specific sugar transport system of the gut, but enhances intracellular metabolic disappearance of glucose thereby creating a larger luminal intracellular concentration gradient which in turn enhances the rate of carrier-facilitated entry.

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.

Contraction-induced increase in muscle insulin sensitivity: requirement for a serum factor

1994 ◽  
Vol 266 (2) ◽  
pp. E186-E192 ◽  
Author(s):  
J. Gao ◽  
E. A. Gulve ◽  
J. O. Holloszy
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Contractile Activity ◽  
Serum Factor ◽  
Enhance Insulin Sensitivity ◽  
Krebs Henseleit Buffer ◽  
Stimulation Of

The insulin sensitivity of glucose transport is enhanced in skeletal muscle after a bout of exercise. In a previous study, stimulation of washed muscles to contract in vitro, in contrast to exercise, did not result in an increase in insulin sensitivity. The purpose of the present study was to explain this apparent discrepancy. We found that, although rat epitrochlearis muscles stimulated to contract in vitro after 15 min of incubation in Krebs-Henseleit buffer did not develop increased insulin sensitivity, muscles stimulated to contract immediately after being dissected showed a small but significant enhancement of the stimulation of 3-O-methyl-D-glucose transport by 30 microU/ml insulin. Furthermore, muscles stimulated to contract in situ and then allowed to recover in vitro showed as large an increase in insulin sensitivity as that which occurs after a bout of swimming. To follow up these findings suggesting involvement of a humoral factor, we incubated epitrochlearis muscles in serum before and during contractile activity in vitro. Epitrochlearis muscle insulin sensitivity was enhanced to as great an extent after in vitro contractile activity in serum as after swimming. Experiments involving charcoal treatment, ultrafiltration, or trypsin digestion provided evidence that the serum factor that interacts with contractions to enhance insulin sensitivity is a protein.

Absorption from gastrointestinal tract of the rat after x-irradiation

1961 ◽  
Vol 201 (6) ◽  
pp. 1013-1016 ◽  
Author(s):  
Maurice F. Sullivan
Keyword(s):  
Nitrogen Mustard ◽  
Direct Action ◽  
Glucose Absorption ◽  
The Other ◽  
Transport Mechanisms ◽  
Passive Transport ◽  
Sugar Absorption ◽  
In Situ Perfusion ◽  
X Irradiation

An in situ perfusion method was used to measure glucose absorption from the x-irradiated or nitrogen-mustard-treated rat. Inhibition was greatest 3 days after treatment and recovery had begun by the 6th day. The effect on absorption was not appreciably different after 900 r than after 1,500 r, although histologic damage was much greater after the higher dose. Pretreatment with cysteine or AET prevented the decreased absorption after 900 r but did not protect against 1,500 r nor against the effect of HN2. The absorption of d(+)-xylose was also decreased 3 days after irradiation of the intestine. Thus, both active and passive transport mechanisms involved in sugar absorption were decreased by irradiation of the intestine. The absorption of fat, on the other hand, was not decreased as a result of direct action by x-radiation on the intestinal epithelium, since oleic acid absorption was unaffected by exposure of the intestine to radiation.

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