Na+-d-glucose Cotransporter SGLT1 is Pivotal for Intestinal Glucose Absorption and Glucose-Dependent Incretin Secretion
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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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L cells can sense carbohydrates via SLC5A1, long-chain fatty acids via FFAR1 and FFAR4 receptors, and monoacylglycerols via the GPR119 receptor.
“L cells can sense carbohydrates via the sodium-coupled glucose transporter (SLC5A1) (Gorboulev et al., 2012;Reimann et al., 2008), long-chain fatty acids via FFAR1 and FFAR4 receptors (Edfalk et al., 2008;Hirasawa et al., 2004), and monoacylglycerols via the GPR119 receptor (Reimann et al., 2008).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Gorboulev et al., 2012
In animals, a wide range of sweet stimuli, including LCS, upregulate SGLT-1 expression and function.
“In animals, a wide range of sweet stimuli are capable of upregulating SGLT-1 expression and function, including LCS (45-48), indicating that SGLT-1 activity is modulated by an upstream and broadly tuned sweet taste sensor.”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [48]
SGLT2 in the S1 and S2 segments of the proximal tubule reabsorbs 90-97% of filtered glucose, whereas SGLT1 in the S3 segment reabsorbs the remaining 3-10%.
“SGLT2 in the S1 and S2 segments of the PT reabsorbs 90 -97% of filtered glucose, whereas SGLT1 in the S3 segment reabsorbs the remaining 3-10% (10,24,27,36,37).”
From Evaluation of renal and cardiovascular protection mechanisms of SGLT2 inhibitors: model-based analysis of clinical data (2018) · cites this paper as [10]
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Self-citationImmediate glucose signaling transmitted via the vagus nerve in gut–brain neural communication
Yamada, S., Natsubori, A., Harada, K., Tsuboi, T., & Monai, H. (2025) · iScience · doi:10.1016/j.isci.2025.112439 · Cited by 7 · see citing works
- Authors
- Gorboulev, V., Schürmann, A., Vallon, V., Kipp, H., Jaschke, A., Klessen, D., Friedrich, A., Scherneck, S., Rieg, T., Cunard, R., Veyhl-Wichmann, M., Srinivasan, A., Balen, D., Breljak, D., Rexhepaj, R., Parker, H. E., Gribble, F. M., Reimann, F., Lang, F., Wiese, S., Sabolic, I., Sendtner, M., & Koepsell, H.
- Affiliations
- University of Würzburg (DE)
- German Institute of Human Nutrition (DE)
- University of California San Diego (US)
- Institute for Medical Research and Occupational Health (HR)
- University of Tübingen (DE)
- Addenbrooke's Hospital (GB)
- Ruhr University Bochum (DE)
- Molecular Toxicology, Institute for Medical Research and Occupational Health, Zagreb, Croatia
- Corresponding author
- Koepsell, Hermann
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2011-12-12
- Volume
- 61
- Issue
- 1
- Pages
- 187-196
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC3237647
- OpenAlex
- W2141228342
- Cited by
- 687
- References
- 45
- Citations by year
- 2026: 31 · 2025: 47 · 2024: 39 · 2023: 33 · 2022: 56 · 2021: 65 · 2020: 49 · 2019: 54 · 2018: 58 · 2017: 51 · 2016: 47 · 2015: 49 · 2014: 42 · 2013: 36 · 2012: 28
- FWCI
- 28.30
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- Apollo (University of Cambridge) (submittedVersion, cc-by-nc-nd)
- Apollo
- Funders
- Wellcome Trust (084210/Z/07/Z, 088357/Z/09/Z, WT088357, #WT084210, 088357, 088357/Z/09/A)
- Deutsche Forschungsgemeinschaft
- Julius-Maximilians-Universität Würzburg
- National Heart, Lung, and Blood Institute (R01HL094728)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK-56248, R01-DK28602, R01DK028602, P30DK079337, R01DK056248)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- SGLT1, intestinal glucose absorption, GLUT2, glucose-galactose malabsorption, glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, incretin secretion, renal glucose reabsorption, brush border membrane
- MeSH terms
- Animals, Female, Glucose, Glycosuria, Intestinal Absorption, Intestine, Small, Kidney Tubules, Proximal, Male, Mice, Inbred C57BL, Oocytes, Mice, Knockout, Insulin-Secreting Cells, Sodium-Glucose Transporter 1, Mice, Incretins
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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