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

Obes Rev. 2013 Nov;14(11):859-70. doi: 10.1111/obr.12063. Epub 2013 Aug 27.

Abstract

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.

Keywords: Food intake; NUCB2; hypothalamus; nesfatin-1.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Appetite Regulation* / genetics
  • Body Weight* / genetics
  • Calcium-Binding Proteins / genetics
  • Calcium-Binding Proteins / physiology*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Forecasting / methods
  • Humans
  • Leptin / genetics
  • Leptin / physiology
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / physiology*
  • Nucleobindins
  • Obesity / etiology
  • Obesity / genetics
  • Obesity / metabolism*
  • Signal Transduction / genetics

Substances

  • Calcium-Binding Proteins
  • DNA-Binding Proteins
  • Leptin
  • NUCB2 protein, human
  • Nerve Tissue Proteins
  • Nucleobindins