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Published on: July 14, 2016
New function for an old enzyme: NEP deficient mice develop late-onset obesity
Matthias Becker1, Wolf-Eberhard Siems, Reinhart Kluge
1Department for Biochemical Neurobiology, Leibniz-Institut für Molekulare Pharmakologie, Berlin, Germany.
Plos One
|September 24, 2010
Summary
Neutral endopeptidase (NEP) deficiency causes obesity by promoting fat accumulation and altering lipid metabolism. This research identifies NEP as a key factor in obesity development, offering a new model for studying this global health issue.
Area of Science:
- Biochemistry
- Metabolic Research
- Obesity Studies
Background:
- The World Health Organization identifies obesity as a global pandemic affecting 300 million people.
- Human obesity is typically polygenic.
- Neutral endopeptidase (NEP), or neprilysin, is a key enzyme in peptide hormone metabolism.
Purpose of the Study:
- To investigate the role of Neutral endopeptidase (NEP) in obesity development.
- To establish NEP-deficient mice as a model for late-onset human obesity.
Main Methods:
- Studied NEP-deficient mice exhibiting late-onset obesity.
- Administered NEP inhibitor candoxatril to wild-type mice.
- Assessed body weight, fat tissue accumulation, lipid metabolism, and glucose tolerance.
Main Results:
- NEP deficiency led to excessive body weight gain due to fat accumulation.
- Mice showed deregulated lipid metabolism and impaired glucose tolerance.
- NEP inhibition increased body weight via enhanced food intake, indicating peripheral action.
- NEP inhibition delayed weight loss in cachectic mice.
Conclusions:
- NEP is a crucial factor in obesity development.
- NEP-deficient mice serve as an ideal model for studying human late-onset obesity.
- This model can advance research into obesity's development, mechanisms, diagnosis, and therapy.
