ABSTRACT
Background: Nesfatin-1, a newly discovered calcium and DNA binding peptide, originate from nucle-obindin 2 [NUCB2] precursors and expressed by central and peripheral nervous system, and peripheral tissues such as digestive organs and adipose tissues. It has the astonishingly large number of chemical messengers for full appetite and introduced as a potential anorectic factor with ability to modulate body weight and probably, energy homeostasis
Nesfatin-1/NUCB2 level in the circulation is elevated after meal intake and decreased during a fast. Its food intake suppression effect is independent from the leptin pathway, and act via the melanocortin signaling. On the other hand, Nesfatin-1 colocalizes with insulin in pancreatic beta islet cells and has been shown to increase insulin secretion
Methodology: PubMed databases were searched for [NUCB2 or nesfatin-1 or nucleobindin] with the combination of [diabetes mellitus]
Included papers were further searched manually for additional studies
The databases were searched up to 2015. Fifty one articles were selected for full text review
Result: Centrally controlled Nesfatin-1 was stated to raise peripheral and hepatic insulin sensitivity by reducing gluconeogenesis and stimulating peripheral glucose uptake in vivo
Conclusion: Nesfatin-1 has gain attention as a new target to generate, drug for treatment of endocrine nutritional and metabolic disorders like obesity and type 2 diabetes mellitus