Low abundance of NPY in the hypothalamus can produce hyperphagia and obesity
In: NPY and cohorts in human disease, proceedings of the 8th international NPY meeting 2006, St. Petersburg, FL, April 22-26, 2006Peptides (New York, NY. 1980) 28(2):475-479; Jg. 28 (2007) 2, S. 475-479
Konferenz
- print, 43 ref
Zugriff:
States of increased metabolic demand are associated with up-regulation of NPY and hyperphagia. However, we present some instances of hyperphagia in which NPY is not up-regulated. Ablation or functional disruption of specific sites in the hypothalamus, such as the ventromedial or paraventricular nuclei, or transection of inputs to the hypothalamus from the hindbrain results in hyperphagia and excess body weight gain. However, NPY expression and concentration in these experimental models is either decreased or unchanged. While there is no up-regulation of NPY in these models, there is increased sensitivity to the orexigenic effects of NPY. This enhanced responsiveness to NPY may more than compensate for the reduced levels of NPY and result in hyperphagia and excess body weight gain. The hyper-responsiveness maybe due either to an increase in NPY receptors or to other changes in target cells and response pathways that may result from the treatments used in these models.
| Titel: |
Low abundance of NPY in the hypothalamus can produce hyperphagia and obesity
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| Autor/in / Beteiligte Person: | DUBE, Michael G ; KALRA, Satya P ; KALRA, Pushpa S |
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| Quelle: | NPY and cohorts in human disease, proceedings of the 8th international NPY meeting 2006, St. Petersburg, FL, April 22-26, 2006Peptides (New York, NY. 1980) 28(2):475-479; Jg. 28 (2007) 2, S. 475-479 |
| Veröffentlichung: | New York, NY: Elsevier Science, 2007 |
| Medientyp: | Konferenz |
| Umfang: | print, 43 ref |
| ISSN: | 0196-9781 (print) |
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