| Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose-dependent incretin secretion. | |
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MedLine Citation:
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PMID: 22124465 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To clarify the physiological role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice were generated and characterized phenotypically. After gavage of d-glucose, small intestinal glucose absorption across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed. Glucose-induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type and Sglt1(-/-) mice were compared. The impact of SGLT1 on renal glucose handling was investigated by micropuncture studies. It was observed that Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome but thrive normally when fed a glucose-galactose-free diet. In wild-type mice, passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1, independent the glucose load. High glucose concentrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulation of GLUT2. SGLT1 was located in luminal membranes of cells immunopositive for GIP and GLP-1, and Sglt1(-/-) mice exhibited reduced glucose-triggered GIP and GLP-1 levels. In the kidney, SGLT1 reabsorbed ∼3% of the filtered glucose under normoglycemic conditions. The data indicate that SGLT1 is 1) pivotal for intestinal mass absorption of d-glucose, 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2. |
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Authors:
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Valentin Gorboulev; Annette Schürmann; Volker Vallon; Helmut Kipp; Alexander Jaschke; Dirk Klessen; Alexandra Friedrich; Stephan Scherneck; Timo Rieg; Robyn Cunard; Maike Veyhl-Wichmann; Aruna Srinivasan; Daniela Balen; Davorka Breljak; Rexhep Rexhepaj; Helen E Parker; Fiona M Gribble; Frank Reimann; Florian Lang; Stefan Wiese; Ivan Sabolic; Michael Sendtner; Hermann Koepsell |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-11-28 |
Journal Detail:
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Title: Diabetes Volume: 61 ISSN: 1939-327X ISO Abbreviation: Diabetes Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-21 Completed Date: 2012-02-13 Revised Date: 2012-05-16 |
Medline Journal Info:
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Nlm Unique ID: 0372763 Medline TA: Diabetes Country: United States |
Other Details:
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Languages: eng Pagination: 187-96 Citation Subset: AIM; IM |
Affiliation:
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Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Female Glucose / pharmacokinetics*, pharmacology Glycosuria / metabolism Incretins / secretion* Insulin-Secreting Cells / drug effects, metabolism Intestinal Absorption / genetics* Intestine, Small / metabolism Kidney Tubules, Proximal / drug effects, metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Oocytes / drug effects, metabolism Sodium-Glucose Transporter 1 / genetics, metabolism, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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088357//Wellcome Trust; P30DK079337/DK/NIDDK NIH HHS; R01 DK056248/DK/NIDDK NIH HHS; R01 HL094728-03/HL/NHLBI NIH HHS; R01DK28602/DK/NIDDK NIH HHS; R01DK56248/DK/NIDDK NIH HHS; R01HL094728/HL/NHLBI NIH HHS; WT084210//Wellcome Trust; WT088357//Wellcome Trust; //Medical Research Council |
| Chemical | |
Reg. No./Substance:
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0/Incretins; 0/Slc5a1 protein, mouse; 0/Sodium-Glucose Transporter 1; 50-99-7/Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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