QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, January 11, 2006, 26(2):389-397; doi:10.1523/JNEUROSCI.1203-05.2006

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Alon, T. Articles by Friedman, J. M. Search for Related Content PubMed PubMed Citation Articles by Alon, T. Articles by Friedman, J. M. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH

 Previous Article  |  Next Article 

Cellular/Molecular
Late-Onset Leanness in Mice with Targeted Ablation of Melanin Concentrating Hormone Neurons

Tamar Alon and Jeffrey M. Friedman

Laboratory of Molecular Genetics, The Rockefeller University, New York, New York 10021

The observation that loss of orexin (hypocretin) neurons causes human narcolepsy raises the possibility that other acquired disorders might also result from loss of hypothalamic neurons. To test this possibility for body weight, mice with selective loss of melanin concentrating hormone (MCH) neurons were generated. MCH was chosen to test because induced mutations of the MCH gene in mice cause hypophagia and leanness. Mice with ablation of MCH neurons were generated using toxin (ataxin-3)-mediated ablation strategy. The mice appeared normal but, after 7 weeks, developed reduced body weight, body length, fat mass, lean mass, and leptin levels. Leanness was characterized by hypophagia and increased energy expenditure. To study the role of MCH neurons on obesity secondary to leptin deficiency, we generated mice deficient in both ob gene product (leptin) and MCH neurons. Absence of MCH neurons in ob/ob mice improved obesity, diabetes, and hepatic steatosis, suggesting that MCH neurons are important mediators of the response to leptin deficiency. These data show that loss of MCH neurons can lead to an acquired leanness. This has implications for the pathogenesis of acquired changes of body weight and might be considered in clinical settings characterized by substantial weight changes later in life.

Key words: MCH; ataxin; leanness; ablation; body weight; energy homeostasis

---

Received March 28, 2005; revised October 24, 2005; accepted October 25, 2005.

This article has been cited by other articles:

				P. Pissios, R. L. Bradley, and E. Maratos-Flier Expanding the Scales: The Multiple Roles of MCH in Regulating Energy Balance and Other Biological Functions Endocr. Rev., October 1, 2006; 27(6): 606 - 620. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help