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Gulay Ciftci

Gulay Ciftci

Ondokuz Mayis University, Turkey

Title: Importance of nesfatin-1 levels in the treatment of obesity

Biography

Biography: Gulay Ciftci

Abstract

Obesity and its associated co-morbidities have become a global health concern. Peptides such as leptin, cholecystokinin, glucagon-like peptide 1 and acylated ghrelin have been shown to influence energy balance in peripheral tissues and brain. It was suggested that nesfatin-1 could play a role in the control of food intake and energy expenditure. Leptin resistance is a common phenomenon in obesity. Central and peripheral injection of nesfatin-1 exerts its food reducing effects via a leptin dependent mechanism. Nesfatin-1 is a recently discovered peptide derived from the precursor protein nucleobindin2 (NUCB2) and described to be expressed in the rat hypothalamus. In quest of novel appetite regulating molecules, NEFA/nucleobindin2, a peroxisome proliferator-γ receptor-activated gene was re-discovered in immortalized cell lines and later in the hypothalamus of rodents. Nesfatin-1 and its precursor NUCB2 possess anorexigenic properties. Nesfatin-1 reduces food intake following central injection in rats, mice or goldfish. Subsequent research showed a more widespread distribution of NUCB2/nesfatin-1 in the rat brain and a prominent expression in the rat stomach with 10-fold higher expression levels in the gastric oxyntic mucosa compared to the brain. A third ventricle injection of either NUCB2 or nesfatin-1 at similar doses reduces food intake in ad libitum fed rats during the dark phase. Moreover, the anorexigenic effect of nesfatin-1 is independent from leptin. Nesfatin-1’s anorexigenic effect was confirmed in further studies where nesfatin-1 was injected centrally in ad libitum fed rats and fasted animals. Whether species differences play a role remains to be further investigated. In summary, current data clearly point towards a role of central nesfatin-1 in the regulation of food intake, whereas peripheral nesfatin-1 seems to be rather involved in the reduction of gastric motility in dogs, increase of hepatic oxidation and glucose homeostasis with an increase of glucose-stimulated insulin release from the pancreas in rats and humans.