GIP, rat
GIP, rat is a bioactive peptide derived from rats. GIP, rat inhibits GIP-mediated postprandial insulin release as well as GIP-promoted glucose uptake in the upper small intestine. GIP, rat can be used in research related to insulin resistance, glucose intolerance, and type 2 diabetes.
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- Fòrmula: C226H343N61O66S
- Peso molecular:5002.58
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
Actividad biológica
GIP, rat (4 h) stimulates cAMP-dependent β-galactosidase production in LGIPR2 cells, with maximum activity observed at a concentration of 10-8 M following 4 h of incubation[5].
GIP, rat binds to GIP receptors on stably transfected L293 cells with an IC50 of 7 nM[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, 250-350 g, fasted for 20 h prior to experimentation, anesthetized with sodium pentobarbital)[3]
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Dosage:0.9 μg immunoreactive rat GIP·kg-1·h-1
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Administration:i.v.; continuous infusion; 90 minutes
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Result:Nearly doubled glucose-induced insulin release, with plasma insulin reaching 178 mU/l at 30 minutes and 171 mU/l at 90 minutes.
Trebled integrated 90-minute insulin response (13.67 mU/mL vs. 4.52 mU/mL for glucose alone).
Significantly reduced integrated 90-minute glucose response (0.28 mol/l vs. 0.53 mol/l for glucose alone).
Raised peak plasma immunoreactive GIP from a basal level of 239 pg/mL to 983 pg/mL at 30 minutes.
Chemical Information
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Peso molecular 5002.58
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Fòrmula C226H343N61O66S
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Sequence
Tyr-Ala-Glu-Gly-Thr-Phe-Ile-Ser-Asp-Tyr-Ser-Ile-Ala-Met-Asp-Lys-Ile-Arg-Gln-Gln-Asp-Phe-Val-Asn-Trp-Leu-Leu-Ala-Gln-Lys-Gly-Lys-Lys-Asn-Asp-Trp-Lys-His-Asn-Leu-Thr-Gln
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Sequence Shortening
YAEGTFISDYSIAMDKIRQQDFVNWLLAQKGKKNDWKHNLTQ
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Tseng CC, et al. Effect of GIP and GLP-1 antagonists on insulin release in the rat. The American journal of physiology. 1999 Jun;276(6):E1049-54. [Content Brief]
[2]. Wewer Albrechtsen NJ, et al. The intestinal distribution pattern of appetite- and glucose regulatory peptides in mice, rats and pigs. BMC research notes. 2016 Feb 02;9:60. [Content Brief]
[3]. Ebert R, et al. Preservation of incretin activity after removal of gastric inhibitory polypeptide (GIP) from rat gut extracts by immunoadsorption. Diabetologia. 1983 Jun;24(6):449-54. [Content Brief]
[4]. Gniuli D, et al. High-fat feeding stimulates endocrine, glucose-dependent insulinotropic polypeptide (GIP)-expressing cell hyperplasia in the duodenum of Wistar rats. Diabetologia. 2010 Oct;53(10):2233-40. [Content Brief]
[5]. Tseng CC, et al. Postprandial stimulation of insulin release by glucose-dependent insulinotropic polypeptide (GIP). Effect of a specific glucose-dependent insulinotropic polypeptide receptor antagonist in the rat. J Clin Invest. 1996 Dec 1;98(11):2440-5. [Content Brief]
[6]. Widenmaier SB, et al. A GIP receptor agonist exhibits beta-cell anti-apoptotic actions in rat models of diabetes resulting in improved beta-cell function and glycemic control. PloS one. 2010 Mar 09;5(3):e9590. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)