Transport and metabolism of glucose by rat small intestine

Glucose transport and metabolism by rat small intestine was investigated by using a preparation for the combined perfusion of the lumen and the vascular bed. 2. When 5 mM-glucose was present in the lumen, only 29% was transported unchanged to the vascular side. Lactate output into the vascular and luminal fluids accounted for a further 53% and 4% respectively of the glucose taken up from the lumen. 3. Glucose was readily taken up when added at 5 mM to the vascular compartment only. Vascular lactate output accounted for approx. 33% of the glucose uptake, and luminal lactate for 6%. 4. When 2 mM-glucose was added to the lumen with 5 mM-glucose in the vascular perfusate, there was no detectable net transport of glucose to the vascular side. However, of the glucose taken up from the lumen, 31% and 2% could be accounted for by increases in vascular and luminal lactate respectively. 5. When 10 mM-glucose was added to the lumen, with 5 mM-glucose in the vascular perfusate, 33% of the glucose disappearing from the lumen was transported to the vascular side. Extra lactate output to the vascular and lumen perfusates accounted for 50% and 9% respectively of the glucose uptake from the lumen. 6. These studies indicate that at low luminal glucose concentrations no sugar is transferred to the blood unchanged, and at sugar concentrations of 5–10 mM only 25–50% of the glucose leaving the lumen reaches the serosal side intact. Furthermore, the small intestine has a greater propensity to form lactate from luminal glucose than from vascular glucose.

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

Diabetes ◽

10.2337/diabetes.42.8.1126 ◽

1993 ◽

Vol 42 (8) ◽

pp. 1126-1132 ◽

Cited By ~ 7

Author(s):

K. L. Madsen ◽

V. M. Porter ◽

R. N. Fedorak

Keyword(s):

Small Intestine ◽

Glucose Transport ◽

Rat Small Intestine

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The effect of vanadate on glucose transport and metabolism in rat small intestine

Biochimica et Biophysica Acta (BBA) - Biomembranes ◽

10.1016/0005-2736(89)90250-2 ◽

1989 ◽

Vol 979 (3) ◽

pp. 311-315 ◽

Cited By ~ 9

Author(s):

George L. Kellett ◽

Elizabeth D. Barker

Keyword(s):

Small Intestine ◽

Glucose Transport ◽

Rat Small Intestine

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Glucocorticoids Enhance Intestinal Glucose Uptake Via the Dimerized Glucocorticoid Receptor in Enterocytes

Endocrinology ◽

10.1210/en.2011-1747 ◽

2012 ◽

Vol 153 (4) ◽

pp. 1783-1794 ◽

Cited By ~ 25

Author(s):

Sybille D. Reichardt ◽

Michael Föller ◽

Rexhep Rexhepaj ◽

Ganesh Pathare ◽

Kerstin Minnich ◽

...

Keyword(s):

Small Intestine ◽

Glucose Uptake ◽

Molecular Mechanism ◽

Glucose Transport ◽

Transcriptional Control ◽

Glucose Transporter ◽

Gene Activation ◽

Mouse Strains ◽

Glucose Transporter 1

Glucocorticoid (GC) treatment of inflammatory disorders, such as inflammatory bowel disease, causes deranged metabolism, in part by enhanced intestinal resorption of glucose. However, the underlying molecular mechanism is poorly understood. Hence, we investigated transcriptional control of genes reported to be involved in glucose uptake in the small intestine after GC treatment and determined effects of GC on electrogenic glucose transport from transepithelial currents. GRvillinCre mice lacking the GC receptor (GR) in enterocytes served to identify the target cell of GC treatment and the requirement of the GR itself; GRdim mice impaired in dimerization and DNA binding of the GR were used to determine the underlying molecular mechanism. Our findings revealed that oral administration of dexamethasone to wild-type mice for 3 d increased mRNA expression of serum- and GC-inducible kinase 1, sodium-coupled glucose transporter 1, and Na+/H+ exchanger 3, as well as electrogenic glucose transport in the small intestine. In contrast, GRvillinCre mice did not respond to GC treatment, neither with regard to gene activation nor to glucose transport. GRdim mice were also refractory to GC, because dexamethasone treatment failed to increase both, gene expression and electrogenic glucose transport. In addition, the rise in blood glucose levels normally observed after GC administration was attenuated in both mutant mouse strains. We conclude that enhanced glucose transport in vivo primarily depends on gene regulation by the dimerized GR in enterocytes, and that this mechanism contributes to GC-induced hyperglycemia.

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Effect of hyperglycemia on d-glucose transport across the brush-border and basolateral membrane of rat small intestine

Biochimica et Biophysica Acta (BBA) - Biomembranes ◽

10.1016/0005-2736(86)90524-9 ◽

1986 ◽

Vol 860 (2) ◽

pp. 277-285 ◽

Cited By ~ 52

Author(s):

D.D. Maenz ◽

C.I. Cheeseman

Keyword(s):

Small Intestine ◽

Glucose Transport ◽

Brush Border ◽

Basolateral Membrane ◽

Rat Small Intestine

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Effect of chronic cold exposure on Na-dependent D-glucose transport along small intestine in ducklings

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.5.r1429 ◽

1996 ◽

Vol 271 (5) ◽

pp. R1429-R1438

Author(s):

V. Thomas ◽

B. Pichon ◽

G. Crouzoulon ◽

H. Barre

Keyword(s):

Small Intestine ◽

Glucose Uptake ◽

Glucose Transport ◽

Cold Exposure ◽

Brush Border ◽

Brush Border Membrane ◽

High Energy ◽

Cold Effect ◽

High Affinity ◽

High Affinity Site

In conditions of chronic cold exposure, ducklings develop a nonshivering thermogenesis that requires a high energy expenditure. Therefore, energy supply becomes essential to cold-acclimated ducklings, which increase their intake of carbohydrate-rich food. The aim of this work was to investigate the effect of cold acclimation on the activity of the intestinal brush-border Na(+)-D-glucose cotransport, which is the first major step controlling glucose entrance into an organism. Cotransport activity was determined by measuring D-glucose uptake in brush-border membrane vesicles isolated from different parts of the small intestine of thermoneutral control (25 degrees C) or cold-acclimated (4 degrees C) ducklings (Cairina moschata). Two D-glucose transport sites were described in ducklings: a high-affinity/low-capacity site and a low-affinity/high-capacity site. The former was mainly located in the ileum and the latter in the duodenum. These two transport sites were altered differently by cold exposure. Major alterations occur in the ileum where 1) a reduction in the Michaelis-Menten constant and maximal transport rate of the high-affinity site was observed, and 2) the occurrence of low-affinity site activity was noted in cold-acclimated ducklings, although it was not detected in the thermoneutral control group. Cold effect on the high-affinity site could be related to the changes in the ileal brush-border membrane vesicle lipids, whereas cold effect on the low-affinity site could be due, at least in part, to the higher glycosyl content found in this segment. The small intestine appears then able to react to cold exposure by increasing both its mucosa mass in proximal segments and D-glucose uptake capacity in ileum to respond to the higher energy demand induced by thermoregulatory requirements.

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