Peptides, enzymes and obesity: New insights from a 'dead' enzyme

Lloyd D. Fricker, Edward H. Leiter

Research output: Contribution to journalReview articlepeer-review

64 Scopus citations


The identification of the fat mutation, which causes obesity in mice, as a defect in carboxypeptidase E (CPE) has raised more questions than answers. CPE is required for the processing of numerous neuroendocrine peptides and a mutation that inactivates CPE was predicted to be lethal. However, Cpe(fat) mutated mice live and become obese. So, why are mice with the Cpe(fat) mutation viable, and why does obesity develop as a consequence of the pleiotropic effects of this mutant allele? Recently, several new members of the carboxypeptidase family have been discovered, of which at least one, CPD, can partially compensate by contributing to neuroendocrine peptide processing. Obesity due to the Cpe(fat) mutation is not caused by increased food consumption but, rather, is a result of defective nutrient partitioning, the exact mechanism of which remains to be elucidated. Copyright (C) 1999 Elsevier Science Ltd.

Original languageEnglish (US)
Pages (from-to)390-393
Number of pages4
JournalTrends in Biochemical Sciences
Issue number10
StatePublished - Oct 1 1999

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


Dive into the research topics of 'Peptides, enzymes and obesity: New insights from a 'dead' enzyme'. Together they form a unique fingerprint.

Cite this