Nucleobindin 2 expression is an independent prognostic factor for bladder cancer.

Nucleobindin 2 (NUCB2) has been reported to play an important role in both tumorigenesis and cancer progression. This study aimed to examine the clinical significance of NUCB2 expression urothelial carcinoma of the bladder (UCB).The expression level of NUCB2 and its correlation with clinicopathological parameters was analyzed in 225 UCB tissues by immunohistochemistry. Kaplan-Meier analysis and Cox proportional hazards regression models were used to investigate the correlation between NUCB2 expression and the prognosis of UCB patients. High NUCB2 expression of UCB patients significantly correlated with aggressive clinicopathological features. Patients with high NUCB2 had shorter overall survival and recurrence-free survival in Kaplan-Meier survival curve (P = .018 and P = .001, respectively).Our results show that high expression of NUCB2 associated with aggressive clinicopathological feature and predicted unfavorable prognosis in patients with UCB might serve as feasible biomarker for clinical outcome of UCB patients after surgery and potential therapeutic target in the future.

Effects of Nesfatin-1 on Food Intake and Hyperglycemia.

Nesfatin-1 is a peptide derived from nucleobindin-2 and involved in the regulation of food intake and hyperglycemia. Nesfatin-1 is a recently described anorexigenic peptide, which may be involved in weight loss, malnutrition, and the regulation of appetite. Nesfatin-1 has an effect on the regulation of glucose homeostasis as well as that of food intake. The aim of this article is to bring a different perspective to the readers on the effects of nesfatin-1 on food intake and hyperglycemia. The central injection of nesfatin-1 may produce anorexigenic effects. The circulating level of nesfatin-1 is thought to be regulated by nutritional status. Long-term changes in body weight can affect nesfatin-1 levels. In overweight and obese individuals, nesfatin-1 levels may increase. Nesfatin-1 is synthesized in the hypothalamic appetite control regions. Nesfatin-1 levels may decrease in individuals with diabetes but may increase in those with impaired glucose tolerance. Nesfatin-1 may have a reducing effect on glucose levels. In addition, an increase in glucose levels may lead to an increase in the release of nesfatin-1 from pancreatic cells. Injection of nesfatin-1 can prevent hepatic glucose formation and stimulate glucose uptake. Reduction of hypothalamic nesfatin-1 levels increases hepatic glucose flow and decreases glucose uptake from peripheral tissues. In the light of all this information, nesfatin-1 may be considered to be an important regulator in the metabolic process. Nesfatin-1 appears to be able to contribute to the treatment of obesity and diabetes because of its anorexigenic and antihyperglycemic effects. Key teaching pointsNesfatin-1 is a anorexigenic peptide.Nesfatin-1 is derived from Nucleobindin-2.Nucleobindin-2 mRNA is produced in different areas of the brain.Nesfatin-1 is an inhibitory factor on appetite and a regulator of energy balance that reduces the increase in body weight.

The first identification of nesfatin-1-expressing neurons in the human bed nucleus of the stria terminalis.

Neuropeptides are involved in various brain activities being able to control a wide spectrum of higher mental functions. The purpose of this concise structural investigation was to detect the possible immunoreactivity of the novel multifunctional neuropeptide nesfatin-1 within the human bed nucleus of the stria terminalis (BNST). The BNST is involved in the mechanism of fear learning, integration of stress and reward circuits, and pathogenesis of addiction. Nesfatin-1-expressing neurons were identified for the first time in several regions of the BNST using both immunohistochemical and fluorescent methods. This may implicate a potential contribution of this neuropeptide to the BNST-related mechanisms of stress/reward responses in the human brain.

Nucleobindin-2/Nesfatin-1 in the Human Hypothalamus Is Reduced in Obese Subjects and Colocalizes with Oxytocin, Vasopressin, Melanin-Concentrating Hormone, and Cocaine- and Amphetamine-Regulated Transcript.

BACKGROUND/AIMS: Nesfatin-1, processed from nucleobindin-2 (NUCB2), is a potent anorexigenic peptide being expressed in rodent hypothalamic nuclei and involved in the regulation of feeding behavior and body weight in animals. The present study aimed to investigate NUCB2/nesfatin-1 protein expression in the human hypothalamus as well as its correlation with body weight. METHODS: Sections of hypothalamus and adjacent cholinergic basal forebrain nuclei, including the nucleus basalis of Meynert (NBM) and the diagonal band of Broca (DBB), from 25 autopsy cases (17 males, 8 females; 8 lean, 9 overweight, 8 obese) were examined using immunohistochemistry and double immunofluorescence labeling. RESULTS: Prominent NUCB2/nesfatin-1 immunoexpression was detected in supraoptic, paraventricular, and infundibular nuclei, lateral hypothalamic area (LHA)/perifornical region, and NBM/DBB. NUCB2/nesfatin-1 was found to extensively colocalize with (a) oxytocin and vasopressin in paraventricular and supraoptic nuclei, (b) melanin-concentrating hormone in the LHA, and (c) cocaine- and amphetamine-regulated transcript in infundibular and paraventricular nuclei and LHA. Interestingly, in the LHA, NUCB2/nesfatin-1 protein expression was significantly decreased in obese, compared with lean (p < 0.01) and overweight (p < 0.05) subjects. CONCLUSIONS: The findings of the present study are suggestive of a potential role for NUCB2/nesfatin-1 as an integral regulator of food intake and energy homeostasis in the human hypothalamus. In the LHA, an appetite- and reward-related brain area, reduced NUCB2/nesfatin-1 immunoexpression may contribute to dysregulation of homeostatic and/or hedonic feeding behavior and obesity. NUCB2/nesfatin-1 localization in NBM/DBB might imply its participation in the neuronal circuitry controlling cognitive influences on food intake and give impetus towards unraveling additional biological actions of NUCB2/nesfatin-1 in human neuronal networks.