The role of the central melanocortin system in the regulation of energy metabolism has received much attention during the past decade since gene mutations of key components in melanocortin signaling cause monogenic forms of obesity in animals and humans. In the arcuate nucleus of the hypothalamus the prohormone proopiomelanocortin (POMC) is posttranslationally cleaved to produce α-melanocyte stimulating hormone (α-MSH), a peptide with anorexigenic effects upon activation of the melanocortin receptors (MCRs). α-MSH undergoes extensive post-translational processing and its in vivo activity is short -lived due to rapid degradation. The enzymatic process that controls α-MSH inactivation is not completely understood. Recent evidence suggests that prolyl carboxypeptidase (PRCP) is an enzyme responsible for α-MSH degradation. PRCP is widely expressed in the body in organs such as the liver, lung, kidney and brain, with a variety of known substrates such as plasma prekallikrein, bradykinin, angiotensins II and III, suggesting its role in the processing of tissue- specific substrates. As with many key melanocortin peptides, gene mutation of PRCP causes a change in the metabolic phenotype of rodents. The purpose of our study is to evaluate the role of PRCP in energy metabolism.

The role of central PRCP in the metabolism regulation

BRUSCHETTA, GIUSEPPE
2017-01-23

Abstract

The role of the central melanocortin system in the regulation of energy metabolism has received much attention during the past decade since gene mutations of key components in melanocortin signaling cause monogenic forms of obesity in animals and humans. In the arcuate nucleus of the hypothalamus the prohormone proopiomelanocortin (POMC) is posttranslationally cleaved to produce α-melanocyte stimulating hormone (α-MSH), a peptide with anorexigenic effects upon activation of the melanocortin receptors (MCRs). α-MSH undergoes extensive post-translational processing and its in vivo activity is short -lived due to rapid degradation. The enzymatic process that controls α-MSH inactivation is not completely understood. Recent evidence suggests that prolyl carboxypeptidase (PRCP) is an enzyme responsible for α-MSH degradation. PRCP is widely expressed in the body in organs such as the liver, lung, kidney and brain, with a variety of known substrates such as plasma prekallikrein, bradykinin, angiotensins II and III, suggesting its role in the processing of tissue- specific substrates. As with many key melanocortin peptides, gene mutation of PRCP causes a change in the metabolic phenotype of rodents. The purpose of our study is to evaluate the role of PRCP in energy metabolism.
23-gen-2017
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3104124
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