Neuropeptide Y in noradrenergic neurons induces obesity in transgenic mouse models.
| Title: | Neuropeptide Y in noradrenergic neurons induces obesity in transgenic mouse models. |
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| Authors: | Vähätalo LH; Department of Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Turku, Finland.; Ruohonen ST; Department of Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Turku, Finland.; Ailanen L; Department of Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Turku, Finland; Drug Research Doctoral Program, University of Turku, Turku, Finland.; Savontaus E; Department of Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Turku, Finland; Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland. Electronic address: eriika.savontaus@utu.fi. |
| Source: | Neuropeptides [Neuropeptides] 2016 Feb; Vol. 55, pp. 31-7. Date of Electronic Publication: 2015 Nov 24. |
| Publication Type: | Journal Article; Research Support, Non-U.S. Gov't; Review |
| Language: | English |
| Journal Info: | Publisher: Elsevier Country of Publication: Netherlands NLM ID: 8103156 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-2785 (Electronic) Linking ISSN: 01434179 NLM ISO Abbreviation: Neuropeptides Subsets: MEDLINE |
| Imprint Name(s): | Publication: 2002- : Amsterdam : Elsevier; Original Publication: Edinburgh ; New York : Churchill Livingstone, c1980- |
| MeSH Terms: | Adrenergic Neurons/*metabolism ; Neuropeptide Y/*metabolism ; Obesity/*metabolism ; Receptors, Neuropeptide Y/*metabolism; Obesity/genetics ; Animals ; Disease Models, Animal ; Humans ; Mice, Transgenic |
| Abstract: | Neuropeptide Y (NPY) in noradrenergic neurons plays an important role in modulating the release and effects of catecholamines in a prolonged stress response. Among other functions, it controls energy metabolism. Transgenic expression of Npy in noradrenergic neurons in mice allowed showing that it is critical for diet- and stress-induced gain in fat mass. When overexpressed, NPY in noradrenergic neurons increases adiposity in gene-dose-dependent fashion, and leads to metabolic disorders such as impaired glucose tolerance. However, the mechanisms of obesity seem to be different in mice heterozygous and homozygous for the Npy transgene. While in heterozygous mice the adipogenic effect of NPY is important, in homozygous mice inhibition of sympathetic tone leading to decreased lipolytic activity and impaired brown fat function, as well as increased endocannabinoid levels contribute to obesity. The mouse model provides novel insight to the mechanisms of human diseases with increased NPY due to chronic stress or gain-of-function gene variants, and a tool for development of novel therapeutics.; (Copyright © 2015 Elsevier Ltd. All rights reserved.) |
| Contributed Indexing: | Keywords: Endocannabinoid system; Glucose metabolism; Hepatosteatosis; Lipid metabolism; Metabolic disorder; Neuropeptide Y; Obesity |
| Substance Nomenclature: | 0 (Neuropeptide Y); 0 (Receptors, Neuropeptide Y) |
| Entry Date(s): | Date Created: 20151219 Date Completed: 20161215 Latest Revision: 20161230 |
| Update Code: | 20260130 |
| DOI: | 10.1016/j.npep.2015.11.088 |
| PMID: | 26681068 |
| Database: | MEDLINE |
Journal Article; Research Support, Non-U.S. Gov't; Review