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Glucose-dependent insulinotropic polypeptide stimulated insulin release from a tumor-derived beta-cell line (beta
T J Kieffer1, C B Verchere, C D Fell
1Department of Physiology, University of British Columbia, Vancouver, Canada.
Abstract:
The beta TC3 tumor cell line was examined for the presence of functional glucose-dependent insulinotropic polypeptide (GIP) receptors. Increasing amounts of natural porcine GIP decreased the binding of HPLC-purified [125I]GIP to beta TC3 cells in a concentration-dependent manner. Displacement of GIP was significant at concentrations as low as 500 pM, and the radioligand was fully displaced at 100 nM. GIP(1-30) produced a displacement of [125I]GIP comparable with that produced by GIP(1-42), and glucagon yielded 20% displacement at a concentration of 1 microM but was without effect at 100 mM. Incubation of beta TC3 cells in the presence of glucose concentrations of 2-20 mM yielded a concentration-dependent stimulation of immunoreactive insulin (IRI) release. GIP and glucagon-like peptide-I(7-36) amide (tGLP-I) at concentrations of 1 nM or greater significantly stimulated IRI release in the presence of 2 mM glucose. The threshold glucose concentration for GIP-stimulated IRI release from beta TC3 cells was 0.5 mM, and maximal potentiation of IRI release by GIP occurred at 5 mM glucose. Somatostatin significantly inhibited GIP-stimulated IRI release in the presence of 5 mM glucose. It is concluded that beta TC3 cells have functional GIP receptors and may provide a useful model for the study of IRI secretion at the cellular level.
Insights
Beta TC3 cells possess functional glucose-dependent insulinotropic polypeptide (GIP) receptors, enabling them to release insulin in response to glucose. This makes them a valuable model for studying insulin secretion at the cellular level.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- The beta TC3 tumor cell line is a pancreatic beta-cell model.
- Understanding the regulation of insulin secretion is crucial for diabetes research.
Purpose of the Study:
- To investigate the presence and function of glucose-dependent insulinotropic polypeptide (GIP) receptors on beta TC3 cells.
- To evaluate the role of GIP in stimulating insulin release from these cells.
Main Methods:
- Radioligand binding assays using [125I]GIP to assess GIP receptor presence.
- Measurement of immunoreactive insulin (IRI) release in response to varying glucose and GIP concentrations.
- Investigating the effects of other peptides like glucagon and somatostatin on insulin release.
Main Results:
- Beta TC3 cells demonstrated specific, concentration-dependent binding of [125I]GIP, indicating functional GIP receptors.
- GIP significantly stimulated IRI release in a glucose-dependent manner, with a threshold at 0.5 mM glucose.
- GIP and tGLP-I enhanced insulin secretion, while somatostatin inhibited GIP-stimulated release.
Conclusions:
- Beta TC3 cells possess functional GIP receptors.
- These cells provide a valuable in vitro model for studying GIP-mediated insulin secretion and the cellular mechanisms involved.