UCP2 mediates ghrelin’s action on NPY/AgRP neurons by lowering free radicals View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-08

AUTHORS

Zane B. Andrews, Zhong-Wu Liu, Nicholas Walllingford, Derek M. Erion, Erzsebet Borok, Jeffery M. Friedman, Matthias H. Tschöp, Marya Shanabrough, Gary Cline, Gerald I. Shulman, Anna Coppola, Xiao-Bing Gao, Tamas L. Horvath, Sabrina Diano

ABSTRACT

The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour. More... »

PAGES

846

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature07181

DOI

http://dx.doi.org/10.1038/nature07181

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047418703

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18668043


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