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.

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.

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.

Comparison of different dietary sugars as inducers of intestinal sugar transporters

1987 ◽  
Vol 252 (4) ◽  
pp. G574-G584 ◽  
Author(s):  
D. H. Solberg ◽  
J. M. Diamond
Keyword(s):  
Small Intestine ◽  
Unit Length ◽  
Sugar Transport ◽  
Dietary Carbohydrate ◽  
Feeding Rates ◽  
Sugar Transporters ◽  
Mouse Small Intestine ◽  
Dietary Fructose ◽  
Carbohydrate Levels ◽  
Dietary Sugars

Intestinal sugar transport increases with dietary carbohydrate levels, but the specific regulatory signals involved have been little studied. Hence we compared rations containing one of five sugars [D-glucose, D-galactose, 3-O-methyl-D-glucose (3-O-MG), D-fructose, and maltose] in their effects on brush-border uptake of five transported solutes (D-glucose, D-galactose, 3-O-MG, D-fructose, and L-proline) by everted sleeves of mouse small intestine. As confirmed by transepithelial potential difference (PD) measurements, there is a distinct fructose transporter that does not evoke a PD, along with one or more aldohexose transporters that do evoke a PD. Galactose and 3-O-MG rations cause a twofold increase in feeding rates, mucosal hyperplasia, and hence nonspecific increases in uptake per unit length of intestine for all transported solutes. Dietary fructose is by far the best specific inducer of the fructose transporter. The five dietary sugars are of fairly similar potency as specific inducers of aldohexose transport, but dietary galactose and fructose may be slightly more potent than glucose. Regulatory signals need not be transported substrates, or vice versa, and need not be metabolizable. Variation in uptake ratios of pairs of aldohexoses with ration and intestinal position suggest multiple aldohexose transporters of overlapping specificity, with different relative activities at different positions and with different susceptibilities to induction by different dietary sugars.

Impaired intestinal and renal glucose transport in PDK-1 hypomorphic mice

2006 ◽  
Vol 291 (5) ◽  
pp. R1533-R1538 ◽  
Author(s):  
Ferruh Artunc ◽  
Rexhep Rexhepaj ◽  
Harald Völkl ◽  
Florian Grahammer ◽  
Christine Remy ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Ussing Chamber ◽  
Glucose Absorption ◽  
Renal Tubules ◽  
Glucose Transporter 1 ◽  
Glucose Reabsorption ◽  
Urinary Glucose ◽  
Proximal Tubular

The phosphoinositide-dependent kinase-1 (PDK-1) activates the serum- and glucocorticoid-inducible kinase and protein kinase B isoforms, which, in turn, are known to stimulate the renal and intestinal Na+-dependent glucose transporter 1. The present study has been performed to explore the role of PDK-1 in electrogenic glucose transport in small intestine and proximal renal tubules. To this end, mice expressing ∼20% of PDK-1 ( pdk1 hm) were compared with their wild-type littermates ( pdk1 wt). According to Ussing chamber experiments, electrogenic glucose transport was significantly smaller in the jejunum of pdk1 hm than of pdk1 wt mice. Similarly, proximal tubular electrogenic glucose transport in isolated, perfused renal tubule segments was decreased in pdk1 hm compared with pdk1 wt mice. Intraperitoneal injection of 3 g/kg body wt glucose resulted in a similar increase of plasma glucose concentration in pdk1 hm and in pdk1 wt mice but led to a higher increase of urinary glucose excretion in pdk1 hm mice. In conclusion, reduction of functional PDK-1 leads to impairment of electrogenic intestinal glucose absorption and renal glucose reabsorption. The experiments disclose a novel element of glucose transport regulation in kidney and small intestine.

Rapid adaptation of intestinal glucose transport: a brush-border or basolateral phenomenon?

1987 ◽  
Vol 253 (1) ◽  
pp. G54-G61 ◽  
Author(s):  
W. H. Karasov ◽  
E. S. Debnam
Keyword(s):  
Glucose Transport ◽  
Brush Border ◽  
Basolateral Membrane ◽  
Glucose Absorption ◽  
Short Time Scale ◽  
Rapid Adaptation ◽  
Significant Difference ◽  
Short Time

Regulation of intestinal nutrient absorption can occur on a very short time scale (i.e., 3–5 h). In this study we set out to determine whether this phenomenon of very rapid adaptation is mediated by changes at the level of the brush-border or basolateral membrane of enterocyte. We employed two experimental manipulations that had been reported to cause increased glucose transport in jejunum within as short a time as 3 h: 1) hyperglycemia caused by jugular vein infusion of glucose, and 2) perfusion of the ileal lumen with glucose. We measured glucose absorption by two methods. 1) An in vitro method that tested directly for an effect at the brush border of enterocytes, and 2) an in vivo method whose measurement is a composite phenomenon including events at both boundaries of enterocytes. Carrier-mediated D-glucose absorption in jejunum in vivo was significantly enhanced by approximately 60% in both experimental situations, but there was no significant difference in in vitro unidirectional uptake at the brush border of tissues removed from the same region of the jejunum. The experimental manipulations also had no effect on glucose uptake by brush-border membranes in the other regions of the gut, nor on the passive uptake of L-glucose or the total uptake of L-proline. These results, plus a comparison of the Vmax values for glucose absorption in vitro and in vivo suggest the following: 1) in the “nonadapted” (i.e., control) rats the rate-limiting step in glucose absorption in vivo is efflux at the basolateral membrane, and 2) the observed rapid increase in glucose absorption in vivo appears to be mediated by change at the level of the basolateral membrane.

Glucose and sorbose absorption at various levels of rat small intestine

1961 ◽  
Vol 200 (2) ◽  
pp. 301-304 ◽  
Author(s):  
R. David Baker ◽  
Gordon W. Searle ◽  
Arthur S. Nunn
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Terminal Ileum ◽  
Glucose Absorption ◽  
Lower Half ◽  
Rat Small Intestine ◽  
Glucose Transfer ◽  
Constant Rate ◽  
Fluoride Poisoning

The passage of glucose and sorbose across the wall at various levels of rat small intestine has been studied in vitro. ‘Uphill’ glucose transport was demonstrated in the jejunum and upper half of the ileum but could not be seen in the terminal quarter of small intestine. Aerobically, in the mid-jejunum glucose absorption from the mucosal solution was about 5.5 times as rapid as in the terminal ileum; the aboral decline in absorptive activity, however, occurred only in the lower half of the small intestine; the upper half absorbed glucose at a nearly constant rate throughout. No aboral decline for rate of glucose transfer into the serosal solution was noticed in the upper three-quarters of small intestine, but in the lower quarter the drop was precipitous. The effects of hypoxia and fluoride poisoning, respectively, on glucose movements were much more severe in the upper than in the lower portions of small intestine. Fluoride (48 mm) completely abolished the absorptive activity gradient for glucose along the small intestine. Sorbose movements were quite similar in rate to the fluoride-inhibited glucose movements.

The level of dietary protein and carbohydrate has a different effect on intestinal uptake of hexoses and lipids in rabbits with an ileal resection than in those with an intact intestinal tract

1987 ◽  
Vol 65 (2) ◽  
pp. 219-225 ◽  
Author(s):  
A. B. R. Thomson
Keyword(s):  
Small Intestine ◽  
Weight Gain ◽  
Dietary Protein ◽  
Body Weight Gain ◽  
Intestinal Transport ◽  
Decanoic Acid ◽  
Ileal Resection ◽  
Low Protein ◽  
Carbohydrate Levels

Either high protein, low carbohydrate (HP) or low protein, high carbohydrate (LP) diets were fed for 6 weeks to rabbits with or without resection of the distal half of the small intestine. Control and resected rabbits fed HP consumed more food and gained more weight than the animals fed LP. The level of dietary protein has a different effect on intestinal transport in animals with an ileal resection than in those with an intact small intestine. With 0.5 mM glucose, the in vitro uptake in control rabbits was greater for the LP than HP diet but was unchanged in resected rabbits; uptake of 0.5 mM galactose and 3-O-methyl glucose was unaffected by HP and LP, whereas in rabbit uptake was lower in LP than HP. The uptake of 40 mM glucose was greater with the LP than HP diet in control rabbits, but lower with LP than HP in resected rabbits. In control rabbits, the uptake of aluric acid was lower on the LP than HP diet; the uptake of octanoic acid, decanoic acid, and cholesterol was unchanged; and the uptake of each fatty acid and cholesterol was greater in resected rabbits fed LP than HP. Feeding a low protein diet to animals with an ileal resection is associated with lower jejunal uptake of high concentrations of glucose, but the higher uptake of glactose and enhanced permeability to fatty acids result in superior weight gain. Thus, recommendations for alterations in dietary protein and carbohydrate levels following ileal resection must be made with the knowledge that these changes may influence intestinal transport function as well as body weight gain.

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
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