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Related Experiment Videos

Disturbed progastrin processing in carboxypeptidase E-deficient fat mice

K A Lacourse1, L Friis-Hansen, J F Rehfeld

  • 1Department of Physiology, University of Michigan, Ann Arbor 48109-0622, USA.

FEBS Letters
|November 22, 1997
PubMed
Summary

A carboxypeptidase E (CPE) mutation impairs progastrin processing in obese mice. Despite this, gastrin synthesis increases, maintaining near-normal bioactive gastrin levels, suggesting alternative G-cell pathways.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Obesity is linked to mutations affecting peptide hormone processing.
  • Carboxypeptidase E (CPE) is crucial for processing regulatory peptides like gastrin.
  • The fat mouse strain has a mutation in the CPE gene, causing obesity.

Purpose of the Study:

  • To investigate progastrin biogenesis and processing in mice with a CPE mutation.
  • To determine the impact of CPE deficiency on gastrin production and its intermediates.

Main Methods:

  • Measurement of gastrin mRNA, carboxyamidated gastrin, and processing intermediates in stomach tissue.
  • Analysis of plasma gastrin concentrations in fasted and postprandial states.

Main Results:

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  • Progastrin processing intermediates, like glycyl-arginine extended gastrin, accumulated significantly (86-fold increase).
  • Total progastrin product and gastrin mRNA levels were doubled in mutant mice.
  • Despite reduced processing efficiency, bioactive gastrin levels were only slightly decreased, and plasma levels were minimally affected.

Conclusions:

  • CPE mutation impairs progastrin processing but stimulates gastrin synthesis to compensate.
  • The unique processing defect in CPE-deficient mice suggests alternative gastrin biosynthetic pathways in G-cells.