Document Detail


Mechanisms of glucose uptake in intestinal cell lines: role of GLUT2.
MedLine Citation:
PMID:  21943636     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: GLUT2 is translocated to the apical membrane of enterocytes exposed to glucose concentrations >∼50 mM. Mechanisms of GLUT2-mediated glucose uptake in cell culture models of enterocytes have not been studied.
AIM: To explore mechanism(s) of glucose uptake in 3 enterocyte-like cell lines.
METHODS: Glucose uptake was measured in Caco-2, RIE-1, and IEC-6 cell lines using varying concentrations of glucose (0.5-50 mM). Effects of phlorizin (SGLT1 inhibitor), phloretin (GLUT2 inhibitor), nocodazole and cytochalasin B (disrupters of cytoskeleton), calphostin C and chelerythrine (PKC inhibitors), and phorbol 12-myristate 13-acetate (PKC activator) were evaluated.
RESULTS: Phlorizin inhibited glucose uptake in all 3 cell lines. Phloretin inhibited glucose uptake in Caco-2 and RIE-1 cells. Starving cells decreased glucose uptake in Caco-2 and RIE-1 cells. Glucose uptake was saturated at >10 mM glucose in all 3 cell lines when exposed briefly (<1 min) to glucose. After exposure for >5 min in Caco-2 and RIE-1 cells, glucose uptake did not saturate and K(m) and V(max) increased. This increase in glucose uptake was inhibited by phloretin, nocodazole, cytochalasin B, calphostin C, and chelerythrine. PMA enhanced glucose uptake by 20%. Inhibitors and PMA had little or no effect in the IEC-6 cells.
CONCLUSION: Constitutive expression of GLUT2 in the apical membrane along with additional translocation of cytoplasmic GLUT2 to the apical membrane via an intact cytoskeleton and activated PKC appears responsible for enhanced carrier-mediated glucose uptake at greater glucose concentrations (>20 mM) in Caco-2 and RIE-1 cells. IEC-6 cells do not appear to express functional GLUT2.
Authors:
Ye Zheng; Jeffrey S Scow; Judith A Duenes; Michael G Sarr
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-09-22
Journal Detail:
Title:  Surgery     Volume:  151     ISSN:  1532-7361     ISO Abbreviation:  Surgery     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-14     Completed Date:  2012-02-08     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0417347     Medline TA:  Surgery     Country:  United States    
Other Details:
Languages:  eng     Pagination:  13-25     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 Mosby, Inc. All rights reserved.
Affiliation:
Department of Surgery and the Gastroenterology Research Unit, Mayo Clinic, Rochester, MN 55905, USA.
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MeSH Terms
Descriptor/Qualifier:
Caco-2 Cells
Cell Differentiation
Cell Polarity
Cytoskeleton / physiology
Enterocytes / cytology,  metabolism*
Glucose / metabolism*
Glucose Transporter Type 2 / metabolism*
Humans
Malabsorption Syndromes / metabolism
Protein Kinase C / metabolism
Sodium-Glucose Transporter 1 / metabolism
Grant Support
ID/Acronym/Agency:
DK-39337/DK/NIDDK NIH HHS; R01 DK039337-18/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Glucose Transporter Type 2; 0/SLC2A2 protein, human; 0/SLC5A1 protein, human; 0/Sodium-Glucose Transporter 1; 50-99-7/Glucose; EC 2.7.11.13/Protein Kinase C
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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