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

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.

Download Full-text

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

Canadian Journal of Biochemistry and Physiology ◽

10.1139/o58-041 ◽

1958 ◽

Vol 36 (3) ◽

pp. 363-371 ◽

Cited By ~ 16

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.

Download Full-text

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

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y58-041 ◽

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.

Download Full-text

Effects of luminal nutrition and metabolic status on in vivo glucose absorption

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.240.6.g432 ◽

1981 ◽

Vol 240 (6) ◽

pp. G432-G436 ◽

Cited By ~ 2

Author(s):

D. P. Kotler ◽

G. M. Levine ◽

Y. F. Shiau

Keyword(s):

Specific Activity ◽

Glucose Absorption ◽

Metabolic Status ◽

Sugar Absorption ◽

Rate Of Absorption ◽

Mucosal Mass ◽

Caloric Balance ◽

Nembutal Anesthesia

Luminal nutrients, but not metabolic status, maintain active glucose transport by the rat intestine in vitro. The present study was designed to examine the effects of these factors on the in vivo absorption of glucose and 3-O-methylglucose. Rats were fed either intraluminally or by total parenteral nutrition (TPN) for 7 days or fasted for 72 h. Sugar absorption was measured under pentobarbital sodium (Nembutal) anesthesia at concentrations from 7 to 28 mM. Luminally fed rats had a significantly greater mucosal mass and absorption rates per centimeter of both sugars than either TPN or fasted animals. However, TPN rats had significantly greater absorption per milligram protein (i.e., specific activity) for both glucose and 3-O-methylglucose than luminally fed rats. In addition, TPN rats absorbed significantly more glucose per milligram protein, but not 3-O-methylglucose, than fasted animals. These data indicate: 1) luminal nutrients maintain glucose absorption by their trophic effects on mucosal mass; 2) the increase in specific activity for sugar absorption after TPN is unrelated to caloric balance; and 3) intestinal glucose metabolism affects its rate of absorption of glucose, but not 3-O-methylglucose.

Download Full-text

Components of Glucose Transport in the Host–Parasite System, Hymenolepis diminuta (Cestoda) and the Rat Intestine

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y74-026 ◽

1974 ◽

Vol 52 (2) ◽

pp. 183-197 ◽

Cited By ~ 21

Author(s):

R. B. Podesta ◽

D. F. Mettrick

Keyword(s):

Glucose Transport ◽

Fluid Transport ◽

Glucose Absorption ◽

Hymenolepis Diminuta ◽

Hydrogen Ion ◽

Ion Concentration ◽

Solvent Drag ◽

Rat Intestine ◽

Hydrogen Ion Concentration

Glucose and fluid transport by the rat intestine and by the tapeworm Hymenolepis diminuta has been studied in vivo, using closed loops of the entire small intestine. The effect of pH, glucose concentration, and the presence of sodium on solute and solvent absorption has been determined in both host and parasite. The effect of the worms on intestinal absorption by the rat has also been evaluated. Three components of the glucose transport system, namely active transport, diffusion, and solvent drag, were determined by means of a model transport equation.Saturation kinetics for glucose absorption did not occur and the absence of sodium in the luminal fluid, while not affecting glucose absorption, markedly reduced fluid absorption by both the intestine and the worms. Lowering the pH of luminal fluids significantly reduced glucose transport by the intestine but increased absorption of fluid and glucose by H. diminuta. Irrespective of pH, fluid and glucose absorption were significantly reduced in the parasitized intestine.Active transport of glucose by normal or parasitized intestine and by H. diminuta was unaffected by the concentration of glucose in the lumen, or by changes in pH. The solvent drag and diffusion components of glucose transport were reduced by increasing the hydrogen ion concentration in uninfected and parasitized intestines. The solvent drag component of glucose absorption by the tapeworms was increased with increasing hydrogen ion concentration.The results are discussed in terms of the current hypotheses on the mechanism of glucose transport, sodium dependency, and the effect of hydrogen ions on transport mechanisms.

Download Full-text

The effect of worm, age, weight and number in the infection on the absorption of glucose by Hymenolepis diminuta

Parasitology ◽

10.1017/s0031182000051817 ◽

1977 ◽

Vol 75 (3) ◽

pp. 277-284 ◽

Cited By ~ 18

Author(s):

D. Henderson

Keyword(s):

Glucose Transport ◽

Transport System ◽

Weight Ratio ◽

Dry Weight ◽

Glucose Absorption ◽

Hymenolepis Diminuta ◽

Glucose Transport System ◽

Rate Of Absorption ◽

Single Worm

SummaryIn Hymenolepis diminuta the in vitro rate of absorption of glucose/unit dry weight of worm falls with increasing worm age, with increasing worm weight and as the number of worms in an infection is increased. In a 6 mM solution of glucose, a 5 mg (dry weight) worm from a 7 or 8 worm infection absorbed 80 µmoles/g dry weight/5 min whereas a 60 mg worm, also from a 7 or 8 worm infection, absorbed only 35µmoles/g dry weight/5 min. This change in the rate of absorption is, at least partly, thought to be due to changes in the relative surface area: weight ratio during growth of the worm.The kinetic parameter, Kt glucose, increased from 1.1 mM for a 5 mg (dry weight) worm from a 7 or 8 worm infection to 2 mM for a 60 mg worm. This change in the functioning of the glucose transport system may indicate that there are two components of the glucose transport system – or two separate systems – one with a low Kt and one with a high Kt, the ratios of which change during worm growth.The smaller the number of worms in an infection the greater the rate of glucose absorption. Using 8–day–old worms in a 6 mM glucose solution, 1 worm from a single worm infection absorbs 111 μmoles/g dry weight/5 min, 1 worm from a 7 or 8 worm infection absorbs 88 μmoles/g dry weight/5 min and 1 worm from a 45–50 worm infection absorbs 77 μmoles/g dry weight/5min. The significance of this is discussed with reference to the ‘crowding effect’ in tapeworms.

Download Full-text

Hepatic uptake of intact glutathione S-conjugate, inhibition by organic anions, and sinusoidal catabolism

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1993.265.3.g547 ◽

1993 ◽

Vol 265 (3) ◽

pp. G547-G554

Author(s):

C. A. Hinchman ◽

A. T. Truong ◽

N. Ballatori

Keyword(s):

Guinea Pig ◽

Rat Liver ◽

Marked Decrease ◽

Hepatic Uptake ◽

Half Time ◽

High Concentrations ◽

Rat Livers ◽

Dose Dependent ◽

Uptake And Metabolism ◽

Guinea Pig Liver

To identify potential mechanisms for hepatic removal of circulating glutathione (GSH) conjugates, uptake and metabolism of S-2,4-dinitrophenylglutathione (DNP-SG) were examined in isolated perfused livers from rat and guinea pig. Guinea pig livers perfused with 5 mumol of DNP-SG in a recirculating system (50 microM initial concn) rapidly cleared the conjugate from the perfusate (half time 3.7 min), whereas clearance was considerably slower in rat liver (half time 35 min). Disappearance of DNP-SG from the perfusate was accompanied by a simultaneous appearance of DNP-SG and its metabolites in bile. Addition of acivicin, an inhibitor of gamma-glutamyltransferase (gamma-GT), to the perfusate resulted in a marked decrease in DNP-SG clearance by guinea pig liver but had no effect in rat liver, suggesting that in the guinea pig this process is largely dependent on sinusoidal gamma-GT activity. However, even in the presence of acivicin, rat and guinea pig livers removed nearly one-half of the administered DNP-SG from the recirculating perfusate over 30 min. High concentrations of DNP-SG were found in bile (up to 3.7 mM), indicating that the liver is capable of transporting the intact conjugate from the circulation. When rat livers were perfused with higher concentrations of DNP-SG (100 and 250 microM), biliary excretion of DNP-SG increased dose dependently, with concentrations in bile reaching 10 mM at the higher dose. This was accompanied by a dose-dependent choleresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Functional expression, quantification and cellular localization of the Hxt2 hexose transporter of Saccharomyces cerevisiae tagged with the green fluorescent protein

Biochemical Journal ◽

10.1042/bj3390299 ◽

1999 ◽

Vol 339 (2) ◽

pp. 299-307 ◽

Cited By ~ 33

Author(s):

Arthur L. KRUCKEBERG ◽

Ling YE ◽

Jan A. BERDEN ◽

Karel van DAM

Keyword(s):

Saccharomyces Cerevisiae ◽

Plasma Membrane ◽

Green Fluorescent Protein ◽

Glucose Transport ◽

Cellular Localization ◽

Fluorescent Protein ◽

Hexose Transporter ◽

High Concentrations ◽

Green Fluorescent

The Hxt2 glucose transport protein of Saccharomyces cerevisiae was genetically fused at its C-terminus with the green fluorescent protein (GFP). The Hxt2-GFP fusion protein is a functional hexose transporter: it restored growth on glucose to a strain bearing null mutations in the hexose transporter genes GAL2 and HXT1 to HXT7. Furthermore, its glucose transport activity in this null strain was not markedly different from that of the wild-type Hxt2 protein. We calculated from the fluorescence level and transport kinetics that induced cells had 1.4×105 Hxt2-GFP molecules per cell, and that the catalytic-centre activity of the Hxt2-GFP molecule in vivo is 53 s-1 at 30 °C. Expression of Hxt2-GFP was induced by growth at low concentrations of glucose. Under inducing conditions the Hxt2-GFP fluorescence was localized to the plasma membrane. In a strain impaired in the fusion of secretory vesicles with the plasma membrane, the fluorescence accumulated in the cytoplasm. When induced cells were treated with high concentrations of glucose, the fluorescence was redistributed to the vacuole within 4 h. When endocytosis was genetically blocked, the fluorescence remained in the plasma membrane after treatment with high concentrations of glucose.

Download Full-text

Comparison of changes evoked by GABA (γ-aminobutyric acid) and anoxia in [K+]o, [Cl-]o, and [Na+]o in stratum pyramidale and stratum radiatum of the guinea pig hippocampus

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y00-001 ◽

2000 ◽

Vol 78 (5) ◽

pp. 378-391 ◽

Cited By ~ 2

Author(s):

G V Obrocea ◽

M E Morris

Keyword(s):

Guinea Pig ◽

Extracellular Space ◽

Hippocampal Slices ◽

Brain Slices ◽

Receptor Activation ◽

Ion Concentration ◽

Aminobutyric Acid ◽

Stratum Radiatum ◽

Bicuculline Methiodide ◽

Stratum Pyramidale

Ion-selective microelectrode recordings were made to assess a possible contribution of extracellular γ-aminobutyric acid (GABA) accumulation to early responses evoked in the brain by anoxia and ischemia. Changes evoked by GABA or N2 in [K+]o, [Cl-]o, [Na+]o, and [TMA+]o were recorded in the cell body and dendritic regions of the stratum pyramidale (SP) and stratum radiatum (SR), respectively, of pyramidal neurons in CA1 of guinea pig hippocampal slices. Bath application of GABA (1-10 mM) for approximately 5 min evoked changes in [K+]o and [Cl-]o with respective EC50 levels of 3.8 and 4.1 mM in SP, and 4.7 and 5.6 mM in SR. In SP 5 mM GABA reversibly increased [K+]o and [Cl-]o and decreased [Na+]o; replacement of 95% O2 -5% CO2 by 95% N2 -5% CO2 for a similar period of time evoked changes which were for each ion in the same direction as those with GABA. In SR both GABA and N2 caused increases in [K+]o and decreases in [Cl-]o and [Na+]o. The reduction of extracellular space, estimated from levels of [TMA+]o during exposures to GABA and N2, was 5-6% and insufficient to cause the observed changes in ion concentration. Ion changes induced by GABA and N2 were reversibly attenuated by the GABAA receptor antagonist bicuculline methiodide (BMI, 100 µM). GABA-evoked changes in [K+]o in SP and SR and [Cl-]o in SP were depressed by >=90%, and of [Cl-]o in SR by 50%; N2-evoked changes in [K+]o in SP and SR were decreased by 70% and those of [Cl-]o by 50%. BMI blocked Δ [Na+]o with both GABA and N2 by 20-30%. It is concluded that during early anoxia: (i) accumulation of GABA and activation of GABAA receptors may contribute to the ion changes and play a significant role, and (ii) responses in the dendritic (SR) regions are greater than and (or) differ from those in the somal (SP) layers. A large component of the [K+]o increase may involve a GABA-evoked Ca2+-activated gk, secondary to [Ca2+]i increase. A major part of [Cl-]o changes may arise from GABA-induced gCl and glial efflux, with strong stimulation of active outward transport and anion exchange at SP, and inward Na+/K+/2Cl- co-transport at SR. Na+ influx is attributable mainly to Na+-dependent transmitter uptake, with only a small amount related to GABAA receptor activation. Although the release and (or) accumulation of GABA during anoxia might be viewed as potentially protectant, the ultimate role may more likely be an important contribution to toxicity and delayed neuronal death. Key words: brain slices, ion-selective microelectrodes, stratum pyramidale, stratum radiatum, bicuculline methiodide, extracellular space shrinkage.

Download Full-text

Regulation of intestinal glucose transport

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y92-167 ◽

1992 ◽

Vol 70 (9) ◽

pp. 1201-1207 ◽

Cited By ~ 26

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.

Download Full-text