Evidence that the major degradation product of glucose-dependent insulinotropic polypeptide, GIP(3-42), is a GIP receptor antagonist in vivo

V.A. Gault, J.C. Parker, Patrick Harriott, P.R. Flatt, F.P.M. O'Harte

Research output: Contribution to journalArticle

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Abstract

The incretin hormone glucose-dependent insulinotropic polypeptide (GIP) is rapidly degraded in the circulation by dipeptidyl peptidase IV forming the N-terminally truncated peptide GIP(3-42). The present study examined the biological activity of this abundant circulating fragment peptide to establish its possible role in GIP action. Human GIP and GIP(3-42) were synthesised by Fmoc solid-phase peptide synthesis, purified by HPLC and characterised by electrospray ionisation-mass spectrometry. In GIP receptor-transfected Chinese hamster lung fibroblasts, GIP(3-42) dose dependently inhibited GIP-stimulated (10(-7) M) cAMP production (up to 75.4 +/-5.4%; P
Original languageEnglish
Pages (from-to)525-533
Number of pages9
JournalJournal of Endocrinology
Volume175
Issue number2
Publication statusPublished - 01 Nov 2002

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Glucose
Peptides
Gastric Inhibitory Polypeptide
Dipeptidyl Peptidase 4
Incretins
Solid-Phase Synthesis Techniques
Peptide Fragments
Electrospray Ionization Mass Spectrometry
Cricetulus
gastric inhibitory polypeptide receptor
Fibroblasts
High Pressure Liquid Chromatography
Hormones
Lung

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Gault, V.A. ; Parker, J.C. ; Harriott, Patrick ; Flatt, P.R. ; O'Harte, F.P.M. / Evidence that the major degradation product of glucose-dependent insulinotropic polypeptide, GIP(3-42), is a GIP receptor antagonist in vivo. In: Journal of Endocrinology. 2002 ; Vol. 175, No. 2. pp. 525-533.
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Evidence that the major degradation product of glucose-dependent insulinotropic polypeptide, GIP(3-42), is a GIP receptor antagonist in vivo. / Gault, V.A.; Parker, J.C.; Harriott, Patrick; Flatt, P.R.; O'Harte, F.P.M.

In: Journal of Endocrinology, Vol. 175, No. 2, 01.11.2002, p. 525-533.

Research output: Contribution to journalArticle

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