Glucose sensing and signalling; regulation of intestinal glucose transport
Open accessAbstract
Epithelial cells lining the inner surface of the intestinal epithelium are in direct contact with a lumenal environment that varies dramatically with diet. It has long been suggested that the intestinal epithelium can sense the nutrient composition of lumenal contents. It is only recently that the nature of intestinal nutrient-sensing molecules and underlying mechanisms have been elucidated. There are a number of nutrient sensors expressed on the luminal membrane of endocrine cells that are activated by various dietary nutrients. We showed that the intestinal glucose sensor, T1R2+T1R3 and the G-protein, gustducin are expressed in endocrine cells. Eliminating sweet transduction in mice in vivo by deletion of either gustducin or T1R3 prevented dietary monosaccharide- and artificial sweetener-induced up-regulation of the Na + /glucose cotransporter, SGLT1 observed in wild-type mice. Transgenic mice, lacking gustducin or T1R3 had deficiencies in secretion of glucagon-like peptide 1 (GLP-1) and, glucose-dependent insulinotrophic peptide (GIP). Furthermore, they had an abnormal insulin profile and prolonged elevation of postprandial blood glucose in response to orally ingested carbohydrates. GIP and GLP-1 increase insulin secretion, while glucagon-like peptide 2 (GLP-2) modulates intestinal growth, blood flow and expression of SGLT1. The receptor for GLP-2 resides in enteric neurons and not in any surface epithelial cells, suggesting the involvement of the enteric nervous system in SGLT1 up-regulation. The accessibility of the glucose sensor and the important role that it plays in regulation of intestinal glucose absorption and glucose homeostasis makes it an attractive nutritional and therapeutic target for manipulation.
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Transport of SGLT-1 monosaccharide substrates triggers incretin hormone secretion, an action attenuated by phlorizin or genetic deletion in rodents.
“Importantly, transport of the monosaccharide substrates of SGLT-1 (e.g., glucose and galactose) triggers incretin hormone secretion (20), an action attenuated when SGLT-1 is pharmacologically inhibited with the competitive antagonist phlorizin, or absent through genetic deletion in rodents (42,43).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [20]
GLP-2 receptors are present on enteric neurons in guinea pig ileum, mouse jejunum, mouse and pig intestine, and absorptive enterocyte progenitors in mouse jejunum respond to GLP-2 in an enteric neuron-dependent manner.
“Indeed, GLP-2 receptors are present on enteric neurons in guinea pig ileum, mouse jejunum, mouse and pig intestine (20,51,52) and absorptive enterocyte progenitors in mouse jejunum respond to GLP-2 in an enteric neuron-dependent manner (52).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [20]
GIP receptor knockout and wild type mice show similar increases in jejunal SGLT-1 expression on a high carbohydrate diet compared to a low carbohydrate diet.
“GIP receptor knockout and wild type mice show similar increases in jejunal SGLT-1 expression on a high carbohydrate diet, compared to mice on a low carbohydrate diet (20).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [20]
GIP is unlikely to be responsible for glucose or LCS effects on SGLT-1.
“While enteric neurons express receptors for other gut hormones, including GIP, GIP is unlikely to be responsible for glucose or LCS effects on SGLT-1 (20,60).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [20]
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- Authors
- Shirazi-Beechey, S. P., Moran, A. W., Batchelor, D. J., Daly, K., & Al-Rammahi, M.
- Affiliations
- University of Liverpool (GB)
- Venue
- Proceedings of the Nutrition Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2011-03-30
- Volume
- 70
- Issue
- 2
- Pages
- 185-193
- ISSN
- 0029-6651 (ISSN-L)
- 1475-2719
- OpenAlex
- W2109762839
- Cited by
- 139
- References
- 83
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 7 · 2023: 10 · 2022: 5 · 2021: 8 · 2020: 6 · 2019: 6 · 2018: 10 · 2017: 14 · 2016: 10 · 2015: 11 · 2014: 15 · 2013: 12 · 2012: 15
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of The Nutrition Society (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pfizer
- Directorate for Biological Sciences
- Biotechnology and Biological Sciences Research Council
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- T1R2/T1R3, gustducin, SGLT1, intestinal endocrine cells, nutrient sensing, glucagon-like peptide-1, glucagon-like peptide-2, insulin secretion, postprandial blood glucose, enteric nervous system, intestinal glucose absorption, glucose homeostasis, artificial sweeteners
- MeSH terms
- Animals, Dietary Carbohydrates, Glucose, Homeostasis, Humans, Intestinal Mucosa, Transducin, Signal Transduction, Enteric Nervous System, Receptors, G-Protein-Coupled, Sodium-Glucose Transporter 1
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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