Cited by 74Gastrointestinal motility and disordersRegulation of Appetite and ObesityBiochemical Analysis and Sensing Techniques

The nutrient-sensing repertoires of mouse enterochromaffin cells differ between duodenum and colon

Martin, A. M., Lumsden, A. L., Young, R. L., Jessup, C. F., Spencer, N. J., Keating, D. J.·2017·Neurogastroenterology & Motility

Abstract

Background: Enterochromaffin (EC) cells within the gastrointestinal (GI) tract provide almost all body serotonin (5‐hydroxytryptamine [5‐HT]). Peripheral 5‐HT, released from EC cells lining the gut wall, serves diverse physiological roles. These include modulating GI motility, bone formation, hepatic gluconeogenesis, thermogenesis, insulin resistance, and regulation of fat mass. Enterochromaffin cells are nutrient sensors, but which nutrients they are responsive to and how this changes in different parts of the GI tract are poorly understood. Methods: To accurately undertake such an examination, we undertook the first isolation and purification of primary mouse EC cells from both the duodenum and colon in the same animal. This allowed us to compare, in an internally controlled manner, regional differences in the expression of nutrient sensors in EC cells using real‐time PCR. Key Results: Both colonic and duodenal EC cells expressed G protein‐coupled receptors and facilitative transporters for sugars, free fatty acids, amino acids, and lipid amides. We find differential expression of nutrient receptor and transporters in EC cells obtained from duodenal and colonic EC cells. Duodenal EC cells have higher expression of tryptophan hydroxylase‐1, sugar transporters GLUT 2, GLUT 5, and free fatty acid receptors 1 and 3 (FFAR 1 and FFAR 3). Colonic EC cells express higher levels of GLUT 1, FFAR 2, and FFAR 4. Conclusions & Inferences: We highlight the diversity of EC cell physiology and identify differences in the regional sensing repertoire of EC cells to an assortment of nutrients. These data indicate that not all EC cells are similar and that differences in their physiological responses are likely dependent on their location within the GI tract.

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Crossref · 10.1111/nmo.13046

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  • Gut-derived 5-HT can modulate glucose and energy homeostasis and is augmented in patients with type 2 diabetes and the obese.

    “Furthermore, gut-derived 5-HT can also modulate glucose and energy homeostasis (68-70), and is augmented in patients with type 2 diabetes (71) and the obese (9).”

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Authors
Martin, A. M., Lumsden, A. L., Young, R. L., Jessup, C. F., Spencer, N. J., & Keating, D. J.
Affiliations
  • Flinders University (AU)
  • South Australian Health and Medical Research Institute (AU)
Corresponding author
Keating, D. J.
Venue
Neurogastroenterology & Motility
Publisher
Wiley
Published
2017-03-02
Volume
29
Issue
6
ISSN
  • 1350-1925 (ISSN-L)
  • 1365-2982
OpenAlex
W2591809802
Cited by
74
References
58
Citations by year
2026: 2 · 2025: 6 · 2024: 6 · 2023: 10 · 2022: 6 · 2021: 12 · 2020: 8 · 2019: 12 · 2018: 10 · 2017: 2
FWCI
9.18
Type
journal article
Language
en
Open access
closed
Locations
  • Neurogastroenterology & Motility (publishedVersion)
  • PubMed (publishedVersion)
  • Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
Funders
  • Australian Research Council
  • National Health and Medical Research Council
Topics
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
Keywords
enterochromaffin cells, nutrient sensing, serotonin, duodenum, colon, regional variation, tryptophan hydroxylase 1, GLUT2, GLUT5, GLUT1, free fatty acid receptors, free fatty acid receptor 1, FFAR3, FFAR2, free fatty acid receptor 4, sugar transporters, amino acid transporters, G protein-coupled receptors, primary cell isolation
MeSH terms
Animals, Colon, Duodenum, Enterochromaffin Cells, Male, Mice, Inbred CBA, Gene Expression, Receptors, G-Protein-Coupled

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