Research Perspective Volume 2, Issue 7 pp 453—456
An animal model manifesting neurodegeneration and obesity
- 1 Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan
- 2 CREST, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan
Received: June 27, 2010 Accepted: July 7, 2010 Published: July 8, 2010
https://doi.org/10.18632/aging.100172How to Cite
Abstract
Although the existence of a link between neurodegenerative diseases and obesity has been suggested, a causal relation between neural degeneration and obesity has remained to be demonstrated experimentally. We recently showed that neurodegeneration in the hypothalamic satiety center results in obesity in mice transgenic for E4B (also known as UFD2a), a mammalian ubiquitin elongation factor (E4). Increased expression of E4B in neurons of the transgenic mice results in the formation of ubiquitin-positive aggregates similar to those apparent in many human neurodegenerative diseases as well as in degeneration of hypothalamic neurons responsible for the regulation of food intake and energy expenditure. We thus propose that neurodegeneration is a possible cause of human obesity and related metabolic diseases, which have become a serious public health problem worldwide. Our animal model is thus a powerful tool for studies of the relation between neurodegeneration and obesity.