OBJECTIVE

The alterations of eating behavior are insufficiently recognized in the clinical attention of adults with obesity. The objective of this study was to examine the characteristics of overeating behavior and its association with depression, perceived stress, acylated ghrelin, nestafin-<em>1</em>, and cortisol.

METHODS

This cross-sectional comparative study included 80 participants with obesity and 50 with normal weight. The volunteers completed questionnaires to evaluate symptoms of food addiction (FA), obsessive compulsive, binge eating (BE), depression, and perceived stress. We measured glucose, lipids, acylated ghrelin, <em>nesfatin</em>-<em>1</em>, and insulin in a fasting blood sample as well as urine cortisol. We compared groups with students t test, and analysis of variance, and tested associations by logistic and multiple regression.

RESULTS

By multiple regression, the BE total score was positively associated with the FA (p < 0.000<em>1</em>) and depression total score (p < 0.000<em>1</em>). By logistic regression, the positive score of FA was associated with ghrelin (p < 0.02). The perceived stress total score was associated negatively with cortisol (p < 0.0006).

CONCLUSIONS

The BE and FA are strongly associated in agreement with the concept that both conditions have overlapping features. Depressive symptoms are associated with symptoms of disordered eating -behavior. FA positive score was associated with ghrelin. BE total score was associated with <em>nesfatin</em>-<em>1</em>.

OBJECTIVE

Malnutrition continues to be a leading cause of stunted growth in many countries. This study aimed to investigate serum <em>nesfatin</em>-<em>1</em> and orexin-A levels in underweight children and the potential correlations of these levels with anthropometric and nutritional parameters.

METHODS

The study enrolled 44 prepubertal children (between 2 and <em>1</em>2 years of age) with thinness grades of <em>1</em>-3 and 4<em>1</em> healthy age- and gender-matched children. The demographic, clinical and laboratory parameters including <em>nesfatin</em>-<em>1</em> and orexin-A concentrations were compared between the two groups. The correlations of <em>nesfatin</em>-<em>1</em> and orexin-A with biochemical and anthropometric parameters were investigated. The receiver operating characteristic (ROC) analysis were also performed for evaluating <em>nesfatin</em>-<em>1</em> and orexin-A in distinguishing children with malnutrition from healthy controls.

RESULTS

Thyroid-stimulating hormone, vitamin B<em>1</em>2 and insulin levels were significantly lower in the study group than controls (p=0.00<em>1</em>, p=0.049 and p=0.033, respectively). Mean <em>nesfatin</em>-<em>1</em> levels in the malnourished group was also significantly lower compared to the healthy controls (387<em>1</em>.2 ± <em>1</em>608.8 vs. 55<em>1</em>5.0 ± 38<em>1</em>6.4 pg/mL, p=0.0<em>1</em>2). No significant difference was observed in the orexin-A levels between the two groups (malnourished vs. control groups: <em>1</em><em>1</em>35.7 ± 306.0 vs. <em>1</em>025.7 ± 36<em>1</em>.6 pg/mL, p=0.<em>1</em>4<em>1</em>). Correlation analyses revealed a positive correlation of <em>nesfatin</em>-<em>1</em> and a negative correlation of orexin-A with body mass index (BMI) z-score. ROC analysis demonstrated that <em>nesfatin</em>-<em>1</em> and orexin-A cannot be used to distinguish children with malnutrition from healthy controls (AUC: 0.620, p=0.06<em>1</em> for <em>nesfatin</em>-<em>1</em> and AUC: 0.584, p=0.<em>1</em>90 for orexin-A).

CONCLUSIONS

The positive correlation of <em>nesfatin</em>-<em>1</em> and the negative correlation of orexin-A with BMI suggest that these neuropeptides may be a part of a protective mechanism in the maintenance of nutritional status and that they may have a role in regulating food intake in undernourished children.

OBJECTIVE

To investigate serum <em>nesfatin</em>-<em>1</em> levels in endometriosis patients.

METHODS

Twenty-five women who were laparoscopically and histopathologically diagnosed with endometriosis (endometriosis group) and 25 women without any pelvic pathology detected by laparoscopy (control group) were enrolled in the study. Serum <em>nesfatin</em>-<em>1</em> levels were compared between the two groups before and after adjustment for body mass index (BMI) and age.

RESULTS

Patients in the endometriosis group had lower BMI than those in the control group (22.3 ± 4.8 kg/m(2) vs. 25.8 ± 4.2 kg/m(2), p=0.009). There was no statistically significant correlation between BMI and serum <em>nesfatin</em>-<em>1</em> levels (p=0.870). Serum <em>nesfatin</em>-<em>1</em> level was statistically significantly lower in the endometriosis group than in the control group (7.2 ± <em>1</em>.3 pg/ml vs. <em>1</em>0.6 ± 2.8 pg/ml, p=0.000<em>1</em>). This result did not change after the adjustment for BMI and age.

CONCLUSIONS

Serum levels of <em>nesfatin</em>-<em>1</em> are decreased in endometriosis patients but its exact role in the etiopathogenesis of endometriosis remains to be clarified.

<em>Nesfatin</em>-<em>1</em>, an anorexigenic peptide derived from nucleobindin 2 (NUCB2), is closely involved in feeding behavior, glycometabolism, and satiety regulation. Some studies show that NUCB2/<em>nesfatin</em>-<em>1</em> is highly expressed and interacts with many appetite-regulating peptides that are co-expressed in the gastrointestinal tract. However, it remains unclear whether <em>nesfatin</em>-<em>1</em> is expressed and interacts similarly in taste buds. Glucagon-like peptide-<em>1</em> (GLP-<em>1</em>), a well-known appetite down-regulating peptide, is associated with changes in the expression of <em>nesfatin</em>-<em>1</em>. Therefore, we measured the expression of the NUCB2 gene and the distribution of <em>nesfatin</em>-<em>1</em>-immunoreactive cells and investigated whether these variables change in taste buds of circumvallate papillae (CV) from rats with type 2 diabetes (T2DM) after treatment with liraglutide, a GLP-<em>1</em> receptor agonist. The results showed that <em>nesfatin</em>-<em>1</em> immunoreactive cells were localized in the taste buds of rat CV. Quantitative RT-PCR showed a significantly lower expression of NUCB2 mRNA in the taste buds of diabetic control rats (T2DM-C) than in those of the normal control group (NC) and a higher level of NUCB2 in the liraglutide treated group (T2DM + LIR) than either the T2DM-C or the NC groups. Changes in the expression of NUCB2 in the rat hypothalamus were opposite to those in CV taste buds. In summary, we found that rat CV taste buds express NUCB2/<em>nesfatin</em>-<em>1</em>, and that this expression decreases significantly in T2DM and increases after treatment with liraglutide in rat CV. This indicates that <em>nesfatin</em>-<em>1</em> could be an important factor in the regulation of gustatory function, feeding and perhaps energy homeostasis.

OBJECTIVE

To observed the post-seizure expression level of neuropeptides ghrelin and <em>Nesfatin</em>-<em>1</em> between the untreated and treated groups in kainic acid-kindling rats and understand the significance of their basic expressions.

METHODS

The male S-D rats were divided randomly into NS and VPA groups after seizure. Each group was divided into 7 subgroups of 3 h, 6 h, <em>1</em>2 h, 24 h, 3 d, 7 d and <em>1</em>4 d. And the blank group (without NS or VPA) and sham group (normal saline instead of kainic acid) were established. RIA (radioimmunoassay), ELISA (enzyme-linked immunosorbent assay) and immunohistochemistry were used to detect the expression levels of ghrelin and <em>Nesfatin</em>-<em>1</em> in the serum and hypothalamus of kainic acid-kindling rats.

RESULTS

Compared with the blank and sham groups, the seizure rats had a decreased expression of ghrelin while there was an elevated expression of <em>Nesfatin</em>-<em>1</em> in hypothalamus. This trend was consistent with the serum expressions of deacylated ghrelin and <em>Nesfatin</em>-<em>1</em>. The expression of ghrelin became elevated at all stages in the VPA group. Especially the subgroups of 24 h (0.320 ± 0.007) and 7 d (0.284 ± 0.004) had a significant increase (P < 0.05) while their expression levels remained lowed than that of the blank group (0.342 ± 0.039). The expressions of <em>Nesfatin</em>-<em>1</em> had a significant decrease (P < 0.05) in all VPA subgroups while they were higher than those in the blank group (0.<em>1</em>24 ± 0.007).

CONCLUSIONS

An accurate detection of serum expression level of deacylated ghrelin and <em>Nesfatin</em>-<em>1</em> may reflect the fluctuation trend of neuropeptides in hypothalamus. It may offer a simple, sensitive and noninvasive method of diagnosing and treating epilepsy.

<em>Nesfatin</em>-<em>1</em> is a neuropeptide localized in hypothalamic paraventricular nucleus (PVN). Previously, we have reported the mechanism of feeding suppression by <em>nesfatin</em>-<em>1</em>, and also reported the ability of <em>nesfatin</em>-<em>1</em> in regulating stress response and the circadian feeding pattern. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide also related to the stress response, feeding, and regulation of cardiovascular and autonomic nervous systems. The neurons with receptors for PACAP are distributed in PVN. However, there are no reports showing the direct effect of PACAP on <em>nesfatin</em>-<em>1</em> neurons. In order to explore the direct effect of PACAP on PVN <em>nesfatin</em>-<em>1</em> neuron, we have measured the cytosolic free calcium ([Ca(2+)]i) using fura-2 microfluorometry in single neurons isolated from PVN of adult rats, followed by immunocytochemical identification of <em>nesfatin</em>-<em>1</em> neurons. PACAP at <em>1</em>0(-<em>1</em>5)M to <em>1</em>0(-9)M increased [Ca(2+)]i in dose dependent manner. PAC<em>1</em> and VPAC2 receptor agonists also increased [Ca(2+)]i. Sixteen out of 40 neurons (40%) in PVN responded to <em>1</em>0(-9)M PACAP, and <em>1</em>2 out of <em>1</em>6 neurons (75%) which responded to <em>1</em>0(-9)M PACAP were found to be <em>nesfatin</em>-<em>1</em> neurons. In this paper we show that PACAP directly activates <em>nesfatin</em>-<em>1</em> neurons in PVN. The data suggest that <em>nesfatin</em>-<em>1</em> controls feeding, stress response or autonomic response under PACAP regulation.

Background/aim: <em>Nesfatin</em>-<em>1</em>, an anorexigenic molecule, seems to play a role in appetite regulation and energy homeostasis. The goal of this study was to evaluate the relation of <em>nesfatin</em>-<em>1</em> with anthropometric and metabolic (ghrelin, leptin) parameters in children with idiopathic chronic malnutrition. Materials and methods: The study included 37 underweight and 38 healthy children who were similar regarding age, sex, and pubertal status. Anthropometric and biochemical (<em>nesfatin</em>-<em>1</em>, ghrelin, and leptin levels) variables were assessed. Results: A total of 37 underweight subjects (mean age <em>1</em>0.5 ± 2.6 years) and 38 heathy subjects (mean age <em>1</em>0.3 ± 2.3 years) were recruited. Underweight children had significantly higher <em>nesfatin</em>-<em>1</em> (2.76 ± 0.4 vs. <em>1</em>.56 ± 0.7, P < 0.00<em>1</em>) and lower leptin levels (2.2<em>1</em> ± 2.0 vs. 5.2<em>1</em> ± 2.4, P < 0.00<em>1</em>) than those of the control subjects. <em>Nesfatin</em>-<em>1</em> levels were significantly associated with only leptin levels, after adjusting for age and BMI (r = –0.37<em>1</em>, P = 0.00<em>1</em>). Conclusion: The present study is the first to evaluate <em>nesfatin</em>-<em>1</em> levels in relation with anthropometric and metabolic parameters in children with chronic malnutrition, who were subsequently found to have significantly higher <em>nesfatin</em>-<em>1</em> levels. Our study underlines that <em>nesfatin</em>-<em>1</em> may play a role in the development of malnutrition by inhibiting food intake in children.

Peripheral anorectic hormones, such as glucagon-like peptide (GLP)-<em>1</em>, cholecystokinin (CCK)-8 and leptin, suppress food intake. The newly-identified anorectic neuropeptide, <em>nesfatin</em>-<em>1</em>, is synthesised in both peripheral tissues and the central nervous system, particularly by various nuclei in the hypothalamus and brainstem. In the present study, we examined the effects of i.p. administration of GLP-<em>1</em> and CCK-8 and co-administrations of GLP-<em>1</em> and leptin at subthreshold doses as confirmed by measurement of food intake, on <em>nesfatin</em>-<em>1</em>-immunoreactive (-IR) neurones in the hypothalamus and brainstem of rats by Fos immunohistochemistry. Intraperitoneal administration of GLP-<em>1</em> (<em>1</em>00 μg/kg) caused significant increases in the number of <em>nesfatin</em>-<em>1</em>-IR neurones expressing Fos-immunoreactivity in the supraoptic nucleus (SON), the area postrema (AP) and the nucleus tractus solitarii (NTS) but not in the paraventricular nucleus (PVN), the arcuate nucleus (ARC) or the lateral hypothalamic area (LHA). On the other hand, i.p. administration of CCK-8 (50 μg/kg) resulted in marked increases in the number of <em>nesfatin</em>-<em>1</em>-IR neurones expressing Fos-immunoreactivity in the SON, PVN, AP and NTS but not in the ARC or LHA. No differences in the percentage of <em>nesfatin</em>-<em>1</em>-IR neurones expressing Fos-immunoreactivity in the nuclei of the hypothalamus and brainstem were observed between rats treated with saline, GLP-<em>1</em> (33 μg/kg) or leptin. However, co-administration of GLP-<em>1</em> (33 μg/kg) and leptin resulted in significant increases in the number of <em>nesfatin</em>-<em>1</em>-IR neurones expressing Fos-immunoreactivity in the AP and the NTS. Furthermore, decreased food intake induced by GLP-<em>1</em>, CCK-8 and leptin was attenuated significantly by pretreatment with i.c.v. administration of antisense <em>nesfatin</em>-<em>1</em>. These results indicate that <em>nesfatin</em>-<em>1</em>-expressing neurones in the brainstem may play an important role in sensing peripheral levels of GLP-<em>1</em> and leptin in addition to CCK-8, and also suppress food intake in rats.

The best known effects of <em>nesfatin</em>-<em>1</em> are on appetite and metabolic regulation. Moreover, several research suggest that <em>nesfatin</em>-<em>1</em> play a role in stress responses. This molecule may be involved in the pathophysiology of mood disorders and suicidal behavior. We compared <em>nesfatin</em>-<em>1</em> levels between depressed patients with suicidal ideation (n = 32, mean ± SD, <em>1</em>,40 ± 0.<em>1</em><em>1</em>), without suicidal ideation(n = 3<em>1</em>, <em>1</em>.46 ± 0.<em>1</em>4) and healthy controls (n = 32, <em>1</em>.52 ± 0.<em>1</em>3). Suicidal ideation was assessed with the Suicide Probability Scale, Scale for Suicide Ideation and depressive symptoms were evaluated with the Hamilton Depression Rating Scale. Blood samples were collected to measure serum <em>nesfatin</em>-<em>1</em>levels by using ELISA method. The study revealed that serum <em>nesfatin</em>-<em>1</em> levels were significantly lower in MDD with suicidal ideation than in healthy volunteers (p < 0.00<em>1</em>). There were a negative correlation between the scores of suicidal ideation and <em>nesfatin</em>-<em>1</em> levels in MDD with SI group (r = -0.2<em>1</em>5; p = 0.0<em>1</em>6). In the future, <em>nesfatin</em>-<em>1</em> levels may one day be applied in predicting and monitoring patients' suicide risk. Further prospective studies are required to elucidate this potential association.

Aim: The aim of this study was to investigate the effect of <em>nesfatin</em>-<em>1</em> signaling in the ventromedial hypothalamus (VMH) on gastric functions, as well as the regulation of these effects by nucleus accumbens (NAc) projections to VMH. Methods: The expression of c-fos in <em>nesfatin</em>ergic VMH neurons induced by gastric distension (GD) was measured using the double fluoro-immunohistochemical staining. The firing rates of neurons were monitored with single-unit extracellular electric discharge recording. The projection of <em>nesfatin</em>ergic neurons from NAc to VMH was observed by fluorogold retrograde tracer combined with fluoro-immunohistochemical staining. The effect of <em>nesfatin</em>-<em>1</em> in VMH or electric stimulation in NAc on gastric function was studied by measuring food intake, gastric acid output, gastric motility, and gastric emptying, and the ability of the melanocortin-3/4 receptor antagonist SHU9<em>1</em><em>1</em>9 or the anti-<em>nesfatin</em>-<em>1</em> antibody to block <em>nesfatin</em>-<em>1</em> in the VMH was assessed. Results: Expression of c-fos was observed in VMH <em>nesfatin</em>ergic neurons following GD in rats. Further, <em>nesfatin</em>-<em>1</em> delivery to single GD-responsive neurons changed the firing rates of these neurons in the VMH. In awake, behaving rats, intra-VMH administration of <em>nesfatin</em>-<em>1</em> inhibited food intake, gastric acid output, gastric motility, and gastric emptying. These effects were abolished by SHU9<em>1</em><em>1</em>9. Fluorogold retrograde tracing showed <em>nesfatin</em>ergic neural projection from the NAc to the VMH. Electrical stimulation of NAc modified the firing rates of the VMH neurons and inhibited food intake and gastric functions. The pretreatment with an anti-<em>nesfatin</em>-<em>1</em> antibody in the VMH reversed the effects of NAc electrical stimulation on the VMH neuronal firing rates and gastric function. Conclusions: <em>Nesfatin</em>-<em>1</em> in the VMH inhibited food intake, gastric acid output, gastric motility, and gastric emptying. A <em>nesfatin</em>ergic pathway between NAc and VMH transmitted metabolism-regulating signals.

BACKGROUND

<em>Nesfatin</em>-<em>1</em>, originating from its precursor protein called nucleobindin 2 (NUCB2), plays an important role in glucose metabolism and diabetes. The aim of this study is to examine the association of the c.<em>1</em>0<em>1</em>2C>G (rs75708<em>1</em>) polymorphism of NUCB2 gene with the presence of T2DM.

METHODS

This study was performed in a population of 396 patients with T2DM and <em>1</em>96 healthy subjects. The c.<em>1</em>0<em>1</em>2C>G polymorphism of NUCB2 gene was determined using polymerase chain reaction and sequencing method.

RESULTS

T2DM patients showed lower CG and GG genotype, as well as G allele frequencies compared with healthy subjects. Logistic regression analysis showed that c.<em>1</em>0<em>1</em>2C>G polymorphism was associated with a decreased risk of developing T2DM. In addition, GG genotype of NUCB2 was significantly correlated with lower levels of body mass index and fasting plasma glucose in patients with T2DM.

CONCLUSIONS

The c.<em>1</em>0<em>1</em>2C>G polymorphism of NUCB2 is associated with the decreased risk of developing T2DM in Chinese Han population.

Anorexigenic protein, <em>nesfatin</em>/nucleobindin-2 (NUCB2) is ubiquitously expressed in peripheral tissues including white adipose tissue. <em>Nesfatin</em>/NUCB2 is selectively expressed in pancreatic β-cell, but not β-cells, β-cells, PP-cells.Starvation significantly increased circulating <em>nesfatin</em>-<em>1</em> concentrations, and refeeding restores the increase by starvation. There is an obvious dissociation in changes between <em>nesfatin</em>-<em>1</em> releases from pancreatic β-cells and circulating <em>nesfatin</em>-<em>1</em>, and an increase of <em>nesfatin</em>-<em>1</em> from pancreatic islets may not be reflected to circulating concentrations of <em>nesfatin</em>-<em>1</em>.<em>Nesfatin</em>-<em>1</em> may be a novel insulinotropic peptide, since endogenous pancreatic islet NUCB2/<em>nesfatin</em> is altered in diabetes and diet-induced obesity. <em>Nesfatin</em>-<em>1</em> may also contribute to the improvement of insulin sensitivity in hyperglycemic state. An increase of circulating <em>nesfatin</em>-<em>1</em>may shift glucose uptake to peripheral organs from skeletal muscles to adipocytes. <em>Nesfatin</em>-<em>1</em> may involve the feedback system from adipocytes to the hypothalamus via general circulation, and from the hypothalamus to adipocytes via sympathetic nervous system. The details of those molecular mechanisms should be clarified by future studies including the analysis of gene targeted animals.

Obesity arises from an impairment of energy homeostasis, which essentially involves the balance of food intake and energy dissipation. Some secreted molecules in the hypothalamus have become the focus of recent attention for their important roles in the regulation of food intake. One such molecule, <em>nesfatin</em>-<em>1</em>, is a novel molecule originally expressed in the hypothalamic nuclei of the brain, which exerts its satiety function in conjunction with other molecules, including oxytocin and pro-opiomelanocortin (POMC). <em>Nesfatin</em>-<em>1</em> is processed from its precursor, DNA binding/EF-hand/acidic protein (NEFA)/nucleobindin 2 (NUCB2), and its mRNA is unexpectedly stabilized by troglitazone, a ligand for peroxisome proliferator-activated receptor γ (PPARγ). Subsequent analyses and observations have demonstrated that <em>nesfatin</em>-<em>1</em> is also located in brain nuclei outside the hypothalamus and in peripheral tissues, and that <em>nesfatin</em>-<em>1</em> neurons in the brain receive several signals. These findings imply that <em>nesfatin</em>-<em>1</em> is an endogenous molecule important for the regulation of not only food intake but also other physiological functions. We discuss what is currently known about <em>nesfatin</em>-<em>1</em>, including new developments in our understanding of its distribution, regulation, and biological function.

The exact mechanisms of polycystic ovary syndrome (PCOS) are unknown and there is no effective cure for the disease. The aim of this study was to evaluate the alterations in serum oestradiol and adiponectin levels and in the expression of some important genes in the uterine and ovarian tissues of PCOS rats. The therapeutic effect of quercetin on PCOS was also assessed. Rats were divided into five groups: control, ethanol, quercetin (Q), PCOS and PCOS+Q. After 30 days of oral treatments, the rats' ovaries and uteri were removed and <em>nesfatin</em>-<em>1</em>, aromatase and adipoR<em>1</em> expressions were quantified with real-time polymerase chain reaction. Serum adiponectin and oestradiol levels were evaluated using enzyme-linked immunosorbent assay technique. The results of this study showed that expression of <em>nesfatin</em>-<em>1</em> and adipoR<em>1</em> genes and adiponectin serum levels decreased in the PCOS rats, but aromatase expression and oestradiol level increased. Treatment with quercetin increased the adiponectin level and expression of adipoR<em>1</em> and <em>nesfatin</em>-<em>1</em> and decreased both the expression of aromatase and the oestradiol level. Quercetin improved PCOS by phytoestrogenic effects and mimicking oestrogen's function. Quercetin also affects important factors in both the uterus and ovary and could improve the obesity and the diabetic and infertility symptoms of PCOS.

<em>Nesfatin</em>-<em>1</em>, encoded by the nucleobindin-2 (NUCB2) gene, is an anorexigenic protein related to energy metabolism, obesity, and insulin resistance. The aim of this study was to evaluate NUCB2 gene polymorphism (rs75708<em>1</em>) and its association with serum levels of <em>nesfatin</em>-<em>1</em> in obese and non-obese women with polycystic ovary syndrome (PCOS). In the study population, we analyzed 60 patients with PCOS and 26 age-matched healthy women as controls. The patients with PCOS were divided into two groups based on body mass index (BMI): obese group (n = 28) or non-obese group (n = 32). NUCB2 was genotyped using the polymerase chain reaction-restriction (PCR) technique. Serum <em>nesfatin</em>-<em>1</em> level was measured by enzyme-linked immunosorbent assay (ELISA). <em>Nesfatin</em>-<em>1</em> levels in the obese PCOS group were significantly lower than those in the non-obese PCOS and control groups (p < 0.00<em>1</em>). There was no statistically significant difference in the distribution of NUCB2 genotypes among the groups (p>> 0.05), whereas <em>nesfatin</em>-<em>1</em> levels in the CC and CG genotypes were lower than those in the GG genotype. <em>Nesfatin</em>-<em>1</em> decreases in PCOS, especially in obese women, and is negatively correlated with cardiometabolic risk factors. Although genotype disturbances of NUCB2 were similar among the groups, CC and CG genotypes accompanied lower <em>nesfatin</em>-<em>1</em> levels. C allele of NUCB2 gene polymorphism and <em>nesfatin</em>-<em>1</em> may play a role in the pathophysiology of PCOS.

<AbstractText>Hashimoto's thyroiditis is the most common autoimmune disorder as cause of secondary hypothyroidism. The disease is associated with several metabolic disturbances and inflammatory disorders.</AbstractText><AbstractText>The aim of the current report was to evaluate several inflammatory and metabolic predictors of Hashimoto's thyroiditis.</AbstractText><AbstractText>In the current study, forty patients with Hashimoto's thyroiditis participated in the current study. They were aged between 20 to 50 years old. Anthropometric and nutritional measurements were assessed and biochemical factors including serum VEGF, IL-23, <em>Nesfatin</em>-<em>1</em> and serum lipids were measured.</AbstractText><AbstractText>Waist circumference was higher among patients with lower serum TSH concentrations. Serum HDL and T4 concentrations were lower and serum IL-23 was higher among patients with higher TSH concentrations. BMI, WC and serum HDL were negative predictors of serum TSH while IL-23 was positively associated with TSH concentrations. Serum lipids including TC, TG and LDL were also negatively associated with T3 and T4 concentrations.</AbstractText><AbstractText>According to our findings, VEGF and serum IL-23 were potent predictors of Hashimoto's thyroiditis. However, further studies are warranted to better clarify these associations and underlying pathologic mechanisms.</AbstractText>

Neurons containing melanin-concentrating hormone (MCH) in the posterior lateral hypothalamus play an integral role in rapid eye movement sleep (REMs) regulation. As MCH neurons also contain a variety of other neuropeptides [e.g., cocaine- and amphetamine-regulated transcript (CART) and <em>nesfatin</em>-<em>1</em>] and neurotransmitters (e.g., glutamate), the specific neurotransmitter responsible for REMs regulation is not known. We hypothesized that glutamate, the primary fast-acting neurotransmitter in MCH neurons, is necessary for REMs regulation. To test this hypothesis, we deleted vesicular glutamate transporter (Vglut2; necessary for synaptic release of glutamate) specifically from MCH neurons by crossing MCH-Cre mice (expressing Cre recombinase in MCH neurons) with Vglut2flox/flox mice (expressing LoxP-modified alleles of Vglut2), and studied the amounts, architecture and diurnal variation of sleep-wake states during baseline conditions. We then activated the MCH neurons lacking glutamate neurotransmission using chemogenetic methods and tested whether these MCH neurons still promoted REMs. Our results indicate that glutamate in MCH neurons contributes to normal diurnal variability of REMs by regulating the levels of REMs during the dark period, but MCH neurons can promote REMs even in the absence of glutamate.

The present review summarizes the current understanding of the neuronal activation patterns induced by <em>nesfatin</em>-<em>1</em> in both the hypothalamus and the brainstem, as well as the physiological outcomes caused by the activation of these neuronal populations. Studies using cFos measurements, Ca(2+) imaging techniques, electrophysiological recordings, and microinjections have led to the identification of the paraventricular nucleus, arcuate nucleus, lateral and ventromedial hypothalamic areas, as well as medullary centers such as the nucleus of the solitary tract and dorsal motor nucleus of the vagus as targets of central <em>nesfatin</em>-<em>1</em> actions on food intake, cardiovascular function, stress responses, and glucose homeostasis.

<em>Nesfatin</em>-<em>1</em> is a recently discovered anorectic protein derived from the precursor nucleobindin-2 (NUCB2). While <em>nesfatin</em>-<em>1</em> has been widely studied in mammals, and goldfish, there are no reports of <em>nesfatin</em>-<em>1</em> in amphibians. Using immunohistochemistry and Western blot analysis, this study assessed the distribution of NUCB2/<em>nesfatin</em>-<em>1</em> in the brain of frog Microhyla ornata. NUCB2/<em>nesfatin</em>-<em>1</em> like immunoreactivity was found in the olfactory receptor neurons, Bowman's glands and in the olfactory epithelium of medial diverticulum. In the brain, immunoreactive perikarya were seen in the anterior preoptic area, magnocellular nucleus, suprachiasmatic nucleus, ventromedial thalamic nucleus, posterior thalamic nucleus, nucleus infundibularis ventralis and dorsalis, and the cerebellar nucleus. NUCB2/<em>nesfatin</em>-<em>1</em>like immunoreactivity was also detected in the pineal and pituitary glands of frog. The presence of NUCB2/<em>nesfatin</em>-<em>1</em> in the key brain regions suggest possible roles for this protein in the regulation of physiological processes in frogs.

The prevalence of obesity is rising worldwide; therefore, the World Health Organization introduced the term 'globesity'. This rise also causes an increase of associated diseases such as cardiovascular diseases, type 2 diabetes, several malignomas as well as psychiatric disorders. In order to face this medical challenge, a better understanding of the pathophysiological alterations under conditions of obesity is necessary. Hunger and satiety are largely regulated by peptidergic hormones predominantly produced in the gastrointestinal tract and signaling to the brain via the gut-brain axis. While several hormones are known to decrease food intake such as <em>nesfatin</em>-<em>1</em>, cholecystokinin (CKK), glucagon-like peptide <em>1</em> (GLP-<em>1</em>), pancreatic polypeptide (PP) and peptide YY (PYY), only one peripherally produced and centrally acting hormone - ghrelin - is known so far that stimulates food intake. Several alterations of the signaling of these hormones have been described in the past years e.g. an attenuated postprandial response of CCK, GLP-<em>1</em> and PYY as well as a reduced postprandial suppression of ghrelin that might contribute to the development and/or maintenance of obesity and will be discussed in the present review. Lastly, gaps in knowledge will be highlighted.

In addition to its anorexigenic properties in the neuroendocrine regulation of hunger and satiety, mounting evidence indicates a role for NUCB2/<em>nesfatin</em>-<em>1</em> in the regulation of emotional stress responses which seems to occur in a sex-specific way. In the present study, we investigated the association of NUCB2/<em>nesfatin</em>-<em>1</em> plasma levels with anxiety, depressiveness and perceived stress in obese men and women and their alterations during inpatient treatment. We expected a decrease of NUCB2/<em>nesfatin</em>-<em>1</em> levels in female and an increase in male patients reporting a relevant alleviation of anxiety. We analyzed 69 inpatients (44 female, 25 male; body mass index, mean: 50.2±9.5kg/m2, range: 3<em>1</em>.8-76.5kg/m2; mean age: 45.0±<em>1</em>2.4years) hospitalized due to morbid obesity with mental (not necessarily anxiety disorders) and somatic comorbidities. NUCB2/<em>nesfatin</em>-<em>1</em> plasma levels were measured by ELISA. Anxiety (GAD-7), depressiveness (PHQ-9) and perceived stress (PSQ-20) were concurrently determined as patient-reported outcomes. All measurements were carried out at the initiation of and during inpatient treatment when a clinically meaningful improvement of anxiety was achieved (≥5 points on GAD-7) or missed (±<em>1</em> point). NUCB2/<em>nesfatin</em>-<em>1</em> was positively correlated with anxiety scores in women at the beginning of (r=0.4<em>1</em><em>1</em>; p=0.006) and during (r=0.30<em>1</em>; p=0.047) inpatient treatment. In men, a significant negative correlation was observed following treatment (r=-0.469; p=0.0<em>1</em>8), while at the outset of treatment only a trend was observed (r=-0.38<em>1</em>; p=0.059). Unexpectedly, neither women (n=<em>1</em>9; at beginning vs. during treatment; 0.49±<em>1</em>.00ng/ml vs. 0.38±0.72ng/ml; p=0.687) nor men (n=9; 0.<em>1</em>7±0.3<em>1</em>ng/ml vs. 0.<em>1</em>9±0.36ng/ml; p=0.427) who improved in anxiety scores (p<0.00<em>1</em>) displayed significant changes of NUCB2/<em>nesfatin</em>-<em>1</em> plasma levels, although the direction of change was as expected with a decrease in women (-23.3%) and an increase in men (+<em>1</em>2.4%). In addition, the change of NUCB2/<em>nesfatin</em>-<em>1</em> was not explained by the course of anxiety (women: p=0.587; men: p=0.373). In conclusion, women and men showed an inverse association between NUCB2/<em>nesfatin</em>-<em>1</em> and anxiety with a positive correlation in women and a negative correlation in men (although this correlation was not statistically significant in men at the beginning of treatment). However, no significant change of NUCB2/<em>nesfatin</em>-<em>1</em> following improvement of anxiety has been observed. This might be due to the short observation interval, or due to too small anxiety improvements associated with too low baseline anxiety levels.

Deoxynivalenol (DON), one of trichothecene mycotoxins produced by the fungus Fusarium, is commonly detected in cereal foods and in secondary food production across the world. Lower concentrations of DON induce a dose-related feed refusal (anorexia), whereas it acts as a potent emetic agent at higher levels. DON-induced emesis in humans and livestock can be observed and recorded in both undeveloped and developed regions such as Lixian, Guide and Huangzhong in China and Illinois in the USA. Some studies with different animal models (pigs and minks) suggested that DON could change expressions of 5-hydroxytryptamine, peptide YY, neuropeptide Y2 receptor and nucleobindin-2/<em>nesfatin</em>-<em>1</em> in plasma and different areas of the brain. Some selective antagonist of 5-hydroxytryptamine 3 receptors can inhibit DON-induced emetic response. Otherwise, the Ca2+ homeostasis and MAPK pathway could be potential directions in future studies. Dolasetron, dantrolene and JNJ-3<em>1</em>020028 can be used in clinical treatment but they have potential toxic effects. (-)Epicatechin, ginger phytochemicals and isoflavone can be tested in in vitro and in vivo for their usage as food additives for reducing the emesis. The present review summarizes and discusses some information from previous and recent prominent publications with the aim to provide some comprehensive and helpful data for understanding the mechanism of DON-induced emesis. Copyright © 20<em>1</em>7 John Wiley & Sons, Ltd.