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

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83 Citations (Scopus)

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

ASJC Scopus subject areas

  • Endocrinology

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