Disturbed progastrin processing in carboxypeptidase E-deficient fat mice.

Abstract:

:The fat mouse strain exhibits a late-onset obesity syndrome associated with a mutation in the gene encoding carboxypeptidase E (CPE). Since CPE plays a central role in the biosynthesis of a number of regulatory peptides, including gastrin, we examined the biogenesis and processing of progastrin in fat/fat mice by measuring gastrin mRNA, carboxyamidated gastrin and its processing intermediates in the stomach. The tissue concentration of carboxyamidated (i.e. bioactive) gastrin was only slightly reduced (601 +/- 28 pmol/g in fat/fat mice vs. 715 +/- 43 pmol/g in wild-type controls). However, progastrin processing intermediates accumulated excessively with an 86-fold increase in the concentration of the CPE substrate, glycyl-arginine extended gastrin, and a seven-fold increase in the concentration of glycine-extended gastrin. Accordingly, the total progastrin product was doubled, as was the concentration of gastrin mRNA. Plasma concentrations of carboxyamidated gastrin were, however slightly reduced both in fasted fat/fat mice and postprandially. The results show that the CPE mutation diminishes the efficiency of progastrin processing, but gastrin synthesis is nevertheless increased to maintain an almost normal production of bioactive gastrins. By comparison with other neuroendocrine prohormones, progastrin processing in CPE-deficient mice is unique. Hence, the increase of glycine-extended gastrin in combination with normal levels of carboxyamidated gastrin suggests that G-cells may have another biosynthetic pathway for gastrin.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Lacourse KA,Friis-Hansen L,Rehfeld JF,Samuelson LC

doi

10.1016/s0014-5793(97)01164-2

subject

Has Abstract

pub_date

1997-10-13 00:00:00

pages

45-50

issue

1

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(97)01164-2

journal_volume

416

pub_type

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