Response to Comment on: Harmancey et al. (2007) Adrenomedullin Inhibits Adipogenesis Under Transcriptional Control of Insulin: Diabetes 56:553–563

  1. Romain Harmancey and
  2. Fatima Smih
  1. From the I2MR Institut National de la Santé Et de La Recherche Médicale (INSERM) U858, Obesity and Heart Failure Team, Université Paul Sabatier (UPS), Institut Louis Bugnard IFR31, Toulouse, France
  1. Address correspondence to Fatima Smih, PhD, I2MR INSERM U858, Obesity and Heart Failure Team, Faculté de Médecine, Université Paul Sabatier, 37 allées Jules Guesde, 31000 Toulouse, France. E-mail: fatima.smih{at}toulouse.inserm.fr

We thank Dr. Takahashi for his interest (1,2). First, the main reason for using 100 nmol/l adrenomedullin was to compensate for the uncontrolled catabolism of exogenously added adrenomedullin. Several reports point out that human adipocytes express neprilysin, one of the main enzymes that degrade adrenomedullin (3,4). The metalloprotease is also expressed by 3T3-F442A preadipocytes during differentiation (R.H., F.S., unpublished data). Moreover, we observed in preliminary experiments that omapatrilat, a dual vasopeptidase inhibitor of neprilysin and ACE, increased adipogenesis in 3T3-F442A preadipocytes.

We also …

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