TY - JOUR
T1 - Peptides, enzymes and obesity
T2 - New insights from a 'dead' enzyme
AU - Fricker, Lloyd D.
AU - Leiter, Edward H.
N1 - Funding Information:
Preparation of this manuscript was supported in part by National Institutes of Health K02 award DA00194 (L. D. F.) and NCRR-PO1-88911 (E. H. L.).
Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1999/10/1
Y1 - 1999/10/1
N2 - 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.
AB - 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.
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U2 - 10.1016/S0968-0004(99)01448-6
DO - 10.1016/S0968-0004(99)01448-6
M3 - Review article
C2 - 10500303
AN - SCOPUS:0033213907
SN - 0968-0004
VL - 24
SP - 390
EP - 393
JO - Trends in Biochemical Sciences
JF - Trends in Biochemical Sciences
IS - 10
ER -