Mechanisms of glucose uptake in intestinal cell lines

Role of GLUT2

Ye Zheng, Jeffrey S. Scow, Judith A. Duenes, Michael G. Sarr

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)13-25
Number of pages13
JournalSurgery
Volume151
Issue number1
DOIs
StatePublished - Jan 2012

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Glucose
Cell Line
Phloretin
Enterocytes
Phlorhizin
Nocodazole
Cytochalasin B
Cytoskeleton
Membranes
Acetates
Cell Culture Techniques

ASJC Scopus subject areas

  • Surgery

Cite this

Zheng, Y., Scow, J. S., Duenes, J. A., & Sarr, M. G. (2012). Mechanisms of glucose uptake in intestinal cell lines: Role of GLUT2. Surgery, 151(1), 13-25. https://doi.org/10.1016/j.surg.2011.07.010

Mechanisms of glucose uptake in intestinal cell lines : Role of GLUT2. / Zheng, Ye; Scow, Jeffrey S.; Duenes, Judith A.; Sarr, Michael G.

In: Surgery, Vol. 151, No. 1, 01.2012, p. 13-25.

Research output: Contribution to journalArticle

Zheng, Y, Scow, JS, Duenes, JA & Sarr, MG 2012, 'Mechanisms of glucose uptake in intestinal cell lines: Role of GLUT2', Surgery, vol. 151, no. 1, pp. 13-25. https://doi.org/10.1016/j.surg.2011.07.010
Zheng, Ye ; Scow, Jeffrey S. ; Duenes, Judith A. ; Sarr, Michael G. / Mechanisms of glucose uptake in intestinal cell lines : Role of GLUT2. In: Surgery. 2012 ; Vol. 151, No. 1. pp. 13-25.
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abstract = "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.",
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AB - 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.

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