Dietary lipids and sweeteners regulate glucagon-like peptide-2 secretion
Abstract
Glucagon-like peptide-2 (GLP-2) is a potent intestinal growth factor derived from enteroendocrine L cells. Although food intake is known to increase GLP-2 secretion, its regulatory mechanisms are largely unknown as a result of its very short half-life in venules. The aims of this study were to compare the effects of luminal nutrients on the stimulation of GLP-2 secretion in vivo using lymph samples and to clarify the involvement of the sweet taste receptor in this process in vitro. Lymph samples were collected from the thoracic duct after bolus administration of dietary lipids or sweetening agents into the duodenum of rats. Human enteroendocrine NCI-H716 cells were also used to compare the effects of various nutrients on GLP-2 secretion. GLP-2 concentrations were measured by ELISA in vivo and in vitro. GLP-2 secretion was enhanced by polyunsaturated fatty acid- and monounsaturated fatty acid-rich dietary oils, dietary carbohydrates, and some kinds of sweeteners in rats; this effect was reproduced in NCI-H716 cells using α-linolenic acid (αLA), glucose, and sweeteners. GLP-2 secretion induced by sweetening agents was inhibited by lactisole, a sweetness-antagonizing inhibitor of T1R3. In contrast, lactisole was unable to inhibit GLP-2 secretion induced by αLA alone. Our results suggested that fatty acid- and sweetener-induced GLP-2 secretion may be mediated by two different pathways, with the sweet taste receptor involved in the regulation of the latter.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
GLP-2 release is STR-dependent in rodents and inhibited by gurmarin.
“This is also true for GLP-2 release, which is STR-dependent in rodents (28,29) and inhibited by the murine STR inhibitor, gurmarin (30).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [28]
STR-dependent release of GLP-1 and GLP-2 is detected at higher concentrations in the portal and lymphatic circulation than the systemic circulation in rodents.
“and STR-dependent release of both GLP-1 and GLP-2 is detected at higher concentrations in the portal and lymphatic circulation than the systemic circulation in rodents (28,53).”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [28]
GLP-2 is capable of upregulating SGLT-1 expression in vivo.
“GLP-2 is also capable of upregulating SGLT-1 expression in vivo (28)”
From Gut mechanisms linking intestinal sweet sensing to glycemic control (2018) · cites this paper as [28]
The citation lists haven’t been fetched yet
References 37 · Cited by 27
- Authors
- Sato, S., Hokari, R., Kurihara, C., Sato, H., Narimatsu, K., Hozumi, H., Ueda, T., Higashiyama, M., Okada, Y., Watanabe, C., Komoto, S., Tomita, K., Kawaguchi, A., Nagao, S., & Miura, S.
- Affiliations
- National Defense Medical College (JP)
- Corresponding author
- Sato, Shingo
- ORCID
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2013-04-15
- Volume
- 304
- Issue
- 8
- Pages
- G708-G714
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2156577390
- Cited by
- 27
- References
- 37
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 6 · 2013: 4
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
- PubMed (publishedVersion)
- 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 › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- glucagon-like peptide-2, dietary fat, dietary sweeteners, sweet taste receptor, T1R3, lactisole, alpha-linolenic acid, polyunsaturated fatty acids, monounsaturated fatty acids, dietary carbohydrates, enteroendocrine L cells, intestinal endocrine cells, NCI-H716 cells, thoracic duct lymph
- MeSH terms
- Animals, Benzene Derivatives, Dietary Carbohydrates, Dietary Fats, Fatty Acids, Monounsaturated, Fatty Acids, Unsaturated, Glucose, Humans, Lymphatic System, Male, Sweetening Agents, Taste, Thoracic Duct, Venules, Rats, Wistar, Enteroendocrine Cells, Cell Line, Tumor, Rats, Glucagon-Like Peptide 2
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 ›
Are you an author, or do you see a problem with this page? Request a review
