Document Detail

Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis.
MedLine Citation:
PMID:  21641553     Owner:  NLM     Status:  In-Data-Review    
Dopaminergic midbrain neurons integrate signals on food palatability and food-associated reward into the complex control of energy homeostasis. To define the role of insulin receptor (IR) signaling in this circuitry, we inactivated IR signaling in tyrosine hydroxylase (Th)-expressing cells of mice (IR(ΔTh)). IR inactivation in Th-expressing cells of mice resulted in increased body weight, increased fat mass, and hyperphagia. While insulin acutely stimulated firing frequency in 50% of dopaminergic VTA/SN neurons, this response was abolished in IR(ΔTh) mice. Moreover, these mice exhibited an altered response to cocaine under food-restricted conditions. Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis.
A Christine Könner; Simon Hess; Sulay Tovar; Andrea Mesaros; Carmen Sánchez-Lasheras; Nadine Evers; Linda A W Verhagen; Hella S Brönneke; André Kleinridders; Brigitte Hampel; Peter Kloppenburg; Jens C Brüning
Related Documents :
22209663 - Antisense reduction of 11β-hydroxysteroid dehydrogenase type 1 enhances energy expendi...
19357223 - Vitamin b-12 and homocysteine status among vegetarians: a global perspective.
9103303 - Diet and colorectal cancer mortality: secular trends over 30 years in 15 european count...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cell metabolism     Volume:  13     ISSN:  1932-7420     ISO Abbreviation:  Cell Metab.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-06-06     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101233170     Medline TA:  Cell Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  720-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Department of Mouse Genetics and Metabolism, Institute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases, Center of Molecular Medicine Cologne, University of Cologne, D-50674 Cologne, Germany; Max Planck Institute for Neurological Research, D-50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine, University Hospital Cologne, D-50924 Cologne, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Protein phosphorylation and prevention of cytochrome oxidase inhibition by ATP: coupled mechanisms o...
Next Document:  FGF15/19 regulates hepatic glucose metabolism by inhibiting the CREB-PGC-1? pathway.