Characterization of GIP(1-30) and GIP(1-42) as stimulators of proinsulin gene transcription.

Abstract:

:Originally characterized in terms of its gastric acid inhibitory properties, GIP (gastric inhibitory polypeptide) expressed in the upper small intestine, was subsequently shown to exert strong glucose-dependent insulin-releasing properties. This action is generally attributed to GIP(1-42) and, so far, no evidence for the contribution of other relevant GIP forms exists. In this study, we compared the effects of GIP(1-42) and C-terminally truncated GIP(1-30) on cAMP production and proinsulin gene transcription at clonal insulin-secreting cell lines (RIN 1046-38, beta TC-3). Both peptides were equally potent stimulators of cAMP generation in both cell lines. Insulin release from RIN 1046-38 cells stimulated by both GIP forms was identical. In both B-cell lines GIP(1-42) and GIP(1-30) stimulated proinsulin gene expression equipotently. GIP not only enhances insulin secretion but also insulin gene expression and, therefore, it is a true insulinotropic hormone.

journal_name

Peptides

journal_title

Peptides

authors

Fehmann HC,Göke B

doi

10.1016/0196-9781(95)00090-7

subject

Has Abstract

pub_date

1995-01-01 00:00:00

pages

1149-52

issue

6

eissn

0196-9781

issn

1873-5169

pii

0196-9781(95)00090-7

journal_volume

16

pub_type

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