PMID: identifiant
de la référence Pubmed : |
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 (17786952) |
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| titre : |
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Sugar sensing by enterocytes combines polarity, membrane bound detectors and sugar metabolism. |
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| auteur(s) : |
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Maude Le Gall ( ) 1, Vanessa Tobin1, Emilie Stolarczyk1, Véronique Dalet1, Armelle Leturque1, Edith Brot-Laroche1 |
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| laboratoire : |
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| 1 : |
Centre de recherche des Cordeliers |
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| INSERM : U872 – Université Pierre et Marie Curie - Paris VI – Université Paris Descartes - Paris V |
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| CRBM des Cordeliers 15, rue de l'ecole de medecine batiment E 75270 Paris cedex 06 |
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| France |
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| résumé : |
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Sugar consumption and subsequent sugar metabolism are known to regulate the expression of genes involved in intestinal sugar absorption and delivery. Here we investigate the hypothesis that sugar-sensing detectors in membranes facing the intestinal lumen or the bloodstream can also modulate intestinal sugar absorption. We used wild-type and GLUT2-null mice, to show that dietary sugars stimulate the expression of sucrase-isomaltase (SI) and L-pyruvate kinase (L-PK) by GLUT2-dependent mechanisms, whereas the expression of GLUT5 and SGLT1, did not rely on the presence of GLUT2. By providing sugar metabolites, sugar transporters, including GLUT2, fuelled a sensing pathway. In Caco2/TC7 enterocytes, we could disconnect the sensing triggered by detector from that produced by metabolism, and found that GLUT2 generated a metabolism-independent pathway to stimulate the expression of SI and L-PK. In cultured enterocytes, both apical and basolateral fructose could increase the expression of GLUT5, conversely, basolateral sugar administration could stimulate the expression of GLUT2. Finally, we located the sweet-taste receptors T1R3 and T1R2 in plasma membranes, and we measured their cognate G alpha Gustducin mRNA levels. Furthermore, we showed that a T1R3 inhibitor altered the fructose-induced expression of SGLT1, GLUT5, and L-PK. Intestinal gene expression is thus controlled by a combination of at least three sugar-signaling pathways triggered by sugar metabolites and membrane sugar receptors that, according to membrane location, determine sugar-sensing polarity. This provides a rationale for how intestine adapts sugar delivery to blood and dietary sugar provision. |
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| domaine : |
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langue du texte
intégral : |
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Anglais |
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| ISSN : |
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0021-9541 |
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| type de publication : |
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Articles dans des revues avec comité de lecture |
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| DOI : |
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10.1002/jcp.21245 |
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| journal : |
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| Journal of Cellular Physiology (J Cell Physiol) |
| Publisher |
John Wiley & Sons |
| ISSN |
0021-9541 (eISSN : 1097-4652) |
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| Audience : |
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internationale |
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| date de publication : |
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12/2007 |
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| volume : |
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213 |
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| numéro : |
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3 |
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| page, identifiant, ... : |
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834-43 |
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| mots-clés auteur : |
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glucose signalling – enterocyte – GLUT2 – sugar metabolism – sweet taste receptor |
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| Descripteur(s) MeSH : |
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Animals – Caco-2 Cells – Cell Polarity – Cloning – Molecular – Enterocytes – Fructose – Glucose – Glucose Transporter Type 2 – Glucose Transporter Type 5 – Green Fluorescent Proteins – Hexoses – Humans – Jejunum – Mice – Inbred C57BL – Knockout – Monosaccharide Transport Proteins – Oligo-1 – 6-Glucosidase – Promoter Regions – Genetic – Protein Structure – Tertiary – RNA – Messenger – Sodium-Glucose Transporter 1 – Sucrase – Sucrose – Sweetening Agents – Transfection |
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| contrat, financement : |
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ALFEDIAM Merck Lipha, Institut Benjamin Delessert, AIP ATC Nutrition; Grant Number: ASEO22129DSA. |
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