Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-09

AUTHORS

Laura E. Parton, Chian Ping Ye, Roberto Coppari, Pablo J. Enriori, Brian Choi, Chen-Yu Zhang, Chun Xu, Claudia R. Vianna, Nina Balthasar, Charlotte E. Lee, Joel K. Elmquist, Michael A. Cowley, Bradford B. Lowell

ABSTRACT

A subset of neurons in the brain, known as 'glucose-excited' neurons, depolarize and increase their firing rate in response to increases in extracellular glucose. Similar to insulin secretion by pancreatic beta-cells, glucose excitation of neurons is driven by ATP-mediated closure of ATP-sensitive potassium (K(ATP)) channels. Although beta-cell-like glucose sensing in neurons is well established, its physiological relevance and contribution to disease states such as type 2 diabetes remain unknown. To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. Here we show that this genetic manipulation impaired the whole-body response to a systemic glucose load, demonstrating a role for glucose sensing by POMC neurons in the overall physiological control of blood glucose. We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes. The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing, and that acute pharmacological inhibition of UCP2 reverses loss of glucose sensing. We conclude that obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited neurons might have a pathogenic role in the development of type 2 diabetes. More... »

PAGES

228

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature06098

DOI

http://dx.doi.org/10.1038/nature06098

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053410928

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17728716


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