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The role of nesfatin-1 in the regulation of food intake and body weight: recent developments and future endeavors


  • A. Stengel,

    1. Charité Center for Internal Medicine and Dermatology, Division for General Internal and Psychosomatic Medicine, Charité- Universitätsmedizin Berlin, Berlin, Germany
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  • M. Mori,

    1. Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Japan
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  • Y. Taché

    Corresponding author
    • Department of Medicine, CURE Digestive Diseases Research Center and Center for Neurobiology of Stress, Digestive Diseases Division UCLA and VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA
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  • Supported by German Research Foundation STE 1765/3-1 (A.S.) and Charité University Funding UFF 89-441-176 (A.S.), NIH R01 DK-33061, NIH Center Grant DK-41301 (Animal Core), VA Research Career Scientist (Y.T.), VA Merit Grant (Y.T.).

Address for correspondence: Professor Y Taché, CURE Building 115, Room 117, VA GLA Healthcare System, 11301 Wilshire Blvd, Los Angeles, CA 90073, USA.



Nesfatin-1 was discovered in 2006 and introduced as a potential novel anorexigenic modulator of food intake and body weight. The past years have witnessed increasing evidence establishing nesfatin-1 as a potent physiological inhibitor of food intake and body weight and unravelled nesfatin-1's interaction with other brain transmitters to exert its food consumption inhibitory effect. As observed for other anorexigenic brain neuropeptides, nesfatin-1 is also likely to exert additional, if not pleiotropic, actions in the brain and periphery. Recent studies established the prominent expression of the nesfatin-1 precursor, nucleobindin2 (NUCB2), in the stomach and pancreas, where nesfatin-1 influences endocrine secretion. This review will highlight the current experimental state-of-knowledge on the effects of NUCB2/nesfatin-1 on food intake, body weight and glucose homeostasis. Potential implications in human obesity will be discussed in relation to the evidence of changes in circulating levels of NUCB2/nesfatin-1 in disease states, the occurrence of genetic NUCB2 polymorphisms and – in contrast to several other hormones – the independence of leptin signalling known to be blunted under conditions of chronically increased body weight.