Expression of taste molecules in the upper gastrointestinal tract in humans with and without type 2 diabetes
Abstract
Objective: Nutrient feedback from the small intestine modulates upper gastrointestinal function and energy intake; however, the molecular mechanism of nutrient detection is unknown. In the tongue, sugars are detected via taste T1R2 and T1R3 receptors and signalled via the taste G-protein α-gustducin (Gα gust ) and the transient receptor potential ion channel, TRPM5. These taste molecules are also present in the rodent small intestine, and may regulate gastrointestinal function. Subjects and methods: Absolute transcript levels for T1R2, T1R3, Gα gust and TRPM5 were quantified in gastrointestinal mucosal biopsies from subjects with and without type 2 diabetes; immunohistochemistry was used to locate Gα gust . Effects of luminal glucose on jejunal expression of taste molecules were also quantified in mice. Results: T1R2, T1R3, Gα gust and TRPM5 were preferentially expressed in the proximal small intestine in humans, with immunolabelling for Gα gust localised to solitary cells dispersed throughout the duodenal villous epithelium. Expression of T1R2, T1R3, TRPM5 (all p<0.05) and Gα gust (p<0.001) inversely correlated with blood glucose concentration in type 2 diabetes subjects but, as a group, did not differ from control subjects. Transcript levels of T1R2 were reduced by 84% following jejunal glucose perfusion in mice (p<0.05). Conclusions: Taste molecules are expressed in nutrient detection regions of the proximal small intestine in humans, consistent with a role in “tasting”. This taste molecule expression is decreased in diabetic subjects with elevated blood glucose concentration, and decreased by luminal glucose in mice, indicating that intestinal “taste” signalling is under dynamic metabolic and luminal control.
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Intestinal STRs are expressed at similar levels in the duodenum in individuals with and without type 2 diabetes when sampled at euglycemia.
“We first established that STRs were expressed at similar levels in the duodenum in both groups when sampled at euglycemia (49).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [49]
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Gut mechanisms linking intestinal sweet sensing to glycemic control
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“We first established that STRs were expressed at similar levels in the duodenum in both groups when sampled at euglycemia (49).”
BackgroundSelf-citation
- Authors
- Young, R. L., Sutherland, K., Pezos, N., Brierley, S. M., Horowitz, M., Rayner, C. K., & Blackshaw, L. A.
- Affiliations
- Hanson Institute (AU)
- Royal Adelaide Hospital (AU)
- National Health and Medical Research Council (AU)
- Corresponding author
- Young, R L
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2008-11-27
- Volume
- 58
- Issue
- 3
- Pages
- 337-346
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- OpenAlex
- W2164578066
- Cited by
- 189
- References
- 40
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 8 · 2020: 14 · 2019: 7 · 2018: 15 · 2017: 13 · 2016: 9 · 2015: 6 · 2014: 19 · 2013: 16 · 2012: 14
- FWCI
- 13.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Gut (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Abbott Laboratories
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- T1R2, T1R3, gustducin, TRPM5, type 2 diabetes, small intestine, nutrient sensing, blood glucose, energy intake regulation
- MeSH terms
- Aged, Animals, Diabetes Mellitus, Type 2, Female, Glucose, Humans, Immunohistochemistry, Jejunum, Male, Mice, Inbred C57BL, Middle Aged, Tongue, Gene Expression, Upper Gastrointestinal Tract, Receptors, G-Protein-Coupled, Mice
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