ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Deletion of prolyl carboxypeptidase attenuates the metabolic effects of diet-induced obesity.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- The 7q11.23 Protein DNAJC30 Interacts with ATP Synthase and Links Mitochondria to Brain Development.Cell · 2018Article
- Expression analysis of candidate genes for fatty acid composition in adipose tissue and identification of regulatory regions.Scientific reports · 2018Article
- Prolylcarboxypeptidase deficiency is associated with increased blood pressure, glomerular lesions, and cardiac dysfunction independent of altered circulating and cardiac angiotensin II.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Obesity is associated with depot-specific alterations in adipocyte DNA methylation and gene expression.Adipocyte · 2017Article
- Article
- POMC Neurons: From Birth to Death.Annual review of physiology · 2017Review
- Systems biology with high-throughput sequencing reveals genetic mechanisms underlying the metabolic syndrome in the Lyon hypertensive rat.Circulation. Cardiovascular genetics · 2015Article
- Participation of the central melanocortin system in metabolic regulation and energy homeostasis.Cellular and molecular life sciences : CMLS · 2014Review
- Quantitative genomics of voluntary exercise in mice: transcriptional analysis and mapping of expression QTL in muscle.Physiological genomics · 2014Article
- Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Prolyl carboxypeptidase mRNA expression in the mouse brain.Brain research · 2014Article
- Prolylcarboxypeptidase independently activates plasma prekallikrein (fletcher factor).Current molecular medicine · 2014Article
- Article
- Prolyl carboxypeptidase and its inhibitors in metabolism.Trends in endocrinology and metabolism: TEM · 2013Article
- Ghrelin regulates hypothalamic prolyl carboxypeptidase expression in mice.Molecular metabolism · 2013Article
- cAMP Elevation Down-Regulates β3 Integrin and Focal Adhesion Kinase and Inhibits Leptin-Induced Migration of MDA-MB-231 Breast Cancer Cells.BioResearch open access · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
α-Melanocyte-stimulating hormone (α-MSH) is a critical regulator of energy metabolism. Prolyl carboxypeptidase (PRCP) is an enzyme responsible for its degradation and inactivation. PRCP-null mice (PRCP(gt/gt)) showed elevated levels of brain α-MSH, reduced food intake, and a leaner phenotype compared with wild-type controls. In addition, they were protected against diet-induced obesity. Here, we show that PRCP(gt/gt) animals have improved metabolic parameters compared with wild-type controls under a standard chow diet (SD) as well as on a high-fat diet (HFD). Similarly to when they are exposed to SD, PRCP(gt/gt) mice exposed to HFD for 13 wk showed a leaner phenotype due to decreased fat mass, increased energy expenditure, and locomotor activity. They also showed improved insulin sensitivity and glucose tolerance compared with WT controls and a significant reduction in fasting glucose levels. These improvements occured before changes in body weight and composition were evident, suggesting that the beneficial effect of PRCP ablation is independent of the adiposity levels. In support of a reduced gluconeogenesis, liver PEPCK and G-6-Pase mRNA levels were reduced significantly in PRCP(gt/gt) compared with WT mice. A significant decrease in liver weight and hepatic triglycerides were also observed in PRCP(gt/gt) compared with WT mice. Altogether, our data suggest that PRCP is an important regulator of energy and glucose homeostasis since its deletion significantly improves metabolic parameters in mice exposed to both SD and HFD.
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