Supported by: German Research Foundation Grants STE 1765/1-1 (A.S.), GO 1718/1-1 (M.G.), VA Research Career Scientist Award, NIHDK 33061, Center Grant DK-41301 (Animal Core) (Y.T.).
Nesfatin-1: a novel inhibitory regulator of food intake and body weight
Article first published online: 10 JUN 2010
© 2010 The Authors. obesity reviews © 2010 International Association for the Study of Obesity
Volume 12, Issue 4, pages 261–271, April 2011
How to Cite
Stengel, A., Goebel, M. and Taché, Y. (2011), Nesfatin-1: a novel inhibitory regulator of food intake and body weight. Obesity Reviews, 12: 261–271. doi: 10.1111/j.1467-789X.2010.00770.x
- Issue published online: 21 MAR 2011
- Article first published online: 10 JUN 2010
- Received 10 March 2010; revised 21 April 2010; accepted 22 April 2010
- Food intake;
- X/A-like cells
The protein nucleobindin 2 (NUCB2) or NEFA (DNA binding/EF-hand/acidic amino acid rich region) was identified over a decade ago and implicated in intracellular processes. New developments came with the report that post-translational processing of hypothalamic NUCB2 may result in nesfatin-1, nesfatin-2 and nesfatin-3 and convergent studies showing that nesfatin-1 and full length NUCB2 injected in the brain potently inhibit the dark phase food intake in rodents including leptin receptor deficient Zucker rats. Nesfatin-1 also reduces body weight gain, suggesting a role as a new anorexigenic factor and modulator of energy balance. In light of the obesity epidemic and its associated diseases, underlying new mechanisms regulating food intake may be promising targets in the drug treatment of obese patients particularly as the vast majority of them display reduced leptin sensitivity or leptin resistance while nesfatin-1's mechanism of action is leptin independent. Although much progress on the localization of NUCB2/nesfatin-1 in the brain and periphery as well as on the understanding of nesfatin-1's anorexic effect have been achieved during the past three years, several important mechanisms have yet to be unraveled such as the identification of the nesfatin-1 receptor and the regulation of NUCB2 processing and nesfatin-1 release.