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Cited by 40Diabetes Treatment and ManagementMetabolism, Diabetes, and CancerPancreatic function and diabetes

Glucose-dependent insulinotropic polypeptide (GIP) stimulates transepithelial glucose transport

Singh, Satish K., Bartoo, Aaron C., Krishnan, Selvi, Boylan, Michael O., Schwartz, John H., Wolfe, M. Michael·2008·Obesity
DOI 10.1038/oby.2008.393
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Abstract

The purpose of this study was to characterize the effects of glucose‐dependent insulinotropic peptide (GIP) on small intestinal glucose transport in vitro. Stripped proximal jejunum from fasted mice was mounted in Ussing chambers. The serosal side was bathed in Regular Ringer solution containing 5 mmol/l glucose, and the mucosal side, with solution containing 10 mmol/l 3‐O‐methyl glucose (3OMG). Intercellular cyclic adenosine monophosphate (cAMP), mucosa‐to‐serosa fluxes of 3OMG (Jms3OMG), and short‐circuit current (ISC) were measured in the presence and absence of GIP. GIP increased cAMP by 2.5‐fold in isolated enterocytes, consistent with a direct effect of GIP on these epithelial cells. GIP also increased ISC and Jms3OMG by 68 and 53%, respectively, indicating that the increase in Jms3OMG was primarily electrogenic, with a small electroneutral component. The stimulatory effect of GIP on Jms3OMG was concentration dependent. In addition, 1,000 nmol/l and 10 nmol/l GIP increased Jms3OMG by 70 and 30% over control, respectively, consistent with receptor activation. Phlorizin (20 μmol/l), an inhibitor of Na+‐glucose cotransporter (SGLT‐1), abolished the increase in I SC and decreased Jms3OMG by ∼65%. These results indicate that stimulation of SGLT‐1 activity by GIP partially accounts for the increase in Jms30MG. These studies are the first to demonstrate direct stimulation of intestinal glucose transport by GIP independent of its insulinotropic properties. GIP stimulates cellular accumulation of cAMP and thereby upregulates glucose transport. The GIP‐induced increase in glucose transport appears to be mediated, at least in part, by SGLT‐1.

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Crossref · 10.1038/oby.2008.393

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  • 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 [60]

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Authors
Singh, S. K., Bartoo, A. C., Krishnan, S., Boylan, M. O., Schwartz, J. H., & Wolfe, M. M.
Affiliations
Boston University (US)
Corresponding author
Singh, Satish K.
ORCID
Venue
Obesity
Publisher
Wiley
Published
2008-11
Volume
16
Issue
11
Pages
2412-2416
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
DOI
10.1038/oby.2008.393
OpenAlex
W2052350377
Cited by
40
References
30
Citations by year
2026: 2 · 2025: 5 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 1 · 2012: 2
FWCI
3.15
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1405 d)
Locations
  • Obesity (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (K08DK002410, R01DK053158, R01 DK53158, R01DK059529)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
glucose-dependent insulinotropic polypeptide, intestinal glucose transport, SGLT1, Na+/glucose cotransport, cAMP signaling, enterocytes, jejunum, short-circuit current, 3-O-methylglucose, phloridzin, GIP receptor, intestinal epithelium
MeSH terms
Cyclic AMP, Animals, Cells, Cultured, Dose-Response Relationship, Drug, Gastric Inhibitory Polypeptide, Gastrointestinal Agents, Glucose, Jejunum, Male, Mice, Inbred BALB C, Obesity, Phlorhizin, 3-O-Methylglucose, Enterocytes, Sodium-Glucose Transporter 1, Mice

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