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Polycystic ovary syndrome (PCOS) is a medical condition that affects the function of the ovaries and hormone production in women. It causes symptoms such as irregular menstruation, increased testosterone secretion, weight gain, excessive hair growth and insulin resistance. The causes are not completely known, but genetic, environmental and lifestyle factors play a role. Possible complications include increased risk of heart disease, diabetes, and high blood pressure. It is diagnosed through laboratory tests, such as examining hormones and white blood cells. Recently, studies are focusing on the level of nesfatin-1 protein in PCOS patients, and the results indicate that its levels differ between patients and healthy people, and it is considered a diagnostic tool that needs extensive study. This study aims: Evaluating the histological changes in the ovaries of women with polycystic ovary syndrome and some vital variables. Materials and working methods: 270 blood samples were collected, divided into two groups. The first group included 180 blood samples from women with polycystic ovary syndrome, and the second group included 90 blood samples from healthy women (control samples). The results between the two groups were carefully evaluated, including evaluating the levels of testosterone and follicle-stimulating hormone. As well as evaluating the level of nesfatin-1 and white blood cells between women with polycystic ovary syndrome and healthy women. Results: Our results showed a relatively high level of nesfatin-1 in polycystic ovary syndrome patients compared to healthy controls. The results showed statistically significant differences at the P≤0.05 level The levels of testosterone, follicle-stimulating hormone, luteinizing hormone, and progesterone also showed an increase in affected patients, and it also showed that there was a significant difference at the p level ≥0.05. While the levels of estrogen (E2) and prolactin showed no significant differences at the level of P>0.05. Women with this syndrome had relatively high white blood cell counts compared to unaffected women. Conclusions: Our results indicate a decreased level of nesfatin-1, as nesfatin-1 is a metabolic regulatory protein. The results also showed an increase in both follicle-stimulating hormone and testosterone and a slight increase in white blood cells, which leads to an imbalance in the regulation of hormones and the menstrual cycle and a threat to the reproductive process. [ABSTRACT FROM AUTHOR]

Calcific aortic valve disease (CAVD) predominantly affects the elderly and currently lacks effective medical treatments. Nesfatin-1, a peptide derived from the cleavage of Nucleobindin 2, has been implicated in various calcification processes, both physiological and pathological. This study explores the impact of Nesfatin-1 on the transformation of aortic valve interstitial cells (AVICs) in CAVD. In vitro experiments showed that Nesfatin-1 treatment mitigated the osteogenic differentiation of AVICs. Corresponding in vivo studies demonstrated a deceleration in the progression of CAVD. RNA-sequencing of AVICs treated with and without Nesfatin-1 highlighted an enrichment of the Ferroptosis pathway among the top pathways identified by the Kyoto Encyclopedia of Genes and Genomes analysis. Further examination confirmed increased ferroptosis in both calcified valves and osteoblast-like AVICs, with a reduction in ferroptosis following Nesfatin-1 treatment. Within the Ferroptosis pathway, ZIP8 showed the most notable modulation by Nesfatin-1. Silencing ZIP8 in AVICs increased ferroptosis and osteogenic differentiation, decreased intracellular Mn2+ concentration, and reduced the expression and activity of superoxide dismutase (SOD2). Furthermore, the silencing of SOD2 exacerbated ferroptosis and osteogenic differentiation. Nesfatin-1 treatment was found to elevate the expression of glutathione peroxidase 4 (GPX4) and levels of glutathione (GSH), as confirmed by Western blotting and GSH concentration assays. In summary, Nesfatin-1 effectively inhibits the osteogenic differentiation of AVICs by attenuating ferroptosis, primarily through the GSH/GPX4 and ZIP8/SOD2 pathways. A schematic model is presented to demonstrate the protective effects of Nesfatin-1 against aortic valve calcification in aortic valve interstitial cells (AVICs). This protection occurs through the regulation of ferroptosis, facilitated by the GSH/GPX4 and ZIP8/SOD2 axes. [Display omitted] • Nesfatin-1 could inhibit AVICs osteogenic differentiation in vitro. • Nesfatin-1 treatment reduces AVICs' osteogenic differentiation, a potential therapy for CAVD. • Ferroptosis is involved in Nesfatin-1 inhibiting AVICs osteogenic differentiation. • GSH/GPX4 and ZIP8/SOD2 axes mediate the reduced ferroptosis level. [ABSTRACT FROM AUTHOR]

It has been recently reported that immune activity of some animal peptides/proteins has been found in some plants. In this study, the presence of immune reactivity of alarin, asprosin, paraoxonase, elabela, glucagon, and nesfatin-1 like molecules was investigated in two plant species related to Kastamonu Taşköprü garlic (an endemic cultivar of the Allium sativum L.) and Tunceli garlic (Allium tuncelianum).10 Kastamonu and 10 Tunceli garlic were embedded in paraffin blocks and 4–5 μm transversal and longitudinal sections were taken and stained by immunohistochemical method. In addition, 500 mg of wet tissue samples were homogenized from these garlic and supernatants were obtained. The amounts of alarin, asprosin, elabela, glucagon and nesfatin-1 were studied by enzyme linked immunosorbent assay (ELISA) method and paraoxonase was studied by spectrophotometric method.Studied molecules show immune reactivity in the cytoplasm of the bulb storage cells of the plants parenchyma. The ELISA supernatant results also confirmed the presence of these animal molecules in the plants.Although we cannot reveal the purpose of the presence of these animal molecules detected in plants with these existing data, we predict that these data will be a source of inspiration in the field of botany, that studies will shift in this direction and that they might contribute to the revision of the evolutionary processes of all living things, especially an ancestor of garlics. [ABSTRACT FROM AUTHOR]

Aims: Cerebral aneurysm (CA) has been considered one of the most common cerebrovascular diseases, affecting millions of people worldwide. A therapeutic agent is currently missing for the treatment of CA. Nesfatin‐1 (Nes‐1) is an 82‐amino acid adipokine which possesses a wide range of biological functions. However, the physiological function of Nes‐1 in CA is still unknown. Here, we aimed to assess the preventive effects of Nes‐1 in the pathological development of CA and elucidate the mechanisms behind this. Methods: We used an elastase‐induced CA model, accompanied by a high‐salt diet to induce hypertension. Additionally, diverse experimental techniques, including Verhoeff‐Van Gieson staining, real time PCR, enzyme‐linked immuno sorbent assay (ELISA), and immunofluorescence staining, were employed to assess CA formation, gene and protein expression, as well as the macrophage infiltration. Results: Our results indicate that administration of Nes‐1 significantly decreased the aneurysm size. Additionally, Nes‐1 prevented inflammatory response by inhibiting the expression of interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), and monocyte chemoattractant protein 1 (MCP‐1) at both the mRNA and protein levels in the Circle of Willis (COW) region. Also, the increased levels of matrix metalloproteinase‐2 (MMP‐2) and matrix metalloproteinase‐9 (MMP‐9) in the COW region were reduced by Nes‐1. We found that Nes‐1 administration suppressed the invasion of macrophages. Mechanistically, Nes‐1 activated Nrf‐2 by promoting its nuclear translocation but prevented the activation of the IκBα/NF‐κB signaling pathway. Conclusion: These findings suggest that Nes‐1 might be used as a promising agent for the prevention of CA. [ABSTRACT FROM AUTHOR]

Nesfatin-1, deriving from a precursor protein, NUCB2, is a newly discovered molecule with anti-apoptotic, anti-inflammatory, antioxidant, and anorexigenic effects. It was initially identified in the central nervous system (CNS) and received increasing interest due to its energy-regulating properties. However, research showed that nesfatin-1 is also expressed in peripheral tissues, including the digestive system. The aim of this review is to give a résumé of the present state of knowledge regarding its structure, immunolocalization, and potential implications in diseases with inflammatory components. The main objective was to focus on its clinical importance as a diagnostic biomarker and potential therapeutic molecule in a variety of disorders, among which digestive disorders were of particular interest. Previous studies have shown that nesfatin-1 regulates the balance between pro- and antioxidant agents, which makes nesfatin-1 a promising therapeutic agent. Further in-depth research regarding the underlying mechanisms of action is needed for a better understanding of its effects. [ABSTRACT FROM AUTHOR]

Background: Adipose tissue is significantly involved in inflammatory bowel disease (IBD). Vitamin D can affect both adipogenesis and inflammation. The aim of this study was to compare the production of selected adipokines, potentially involved in the pathogenesis of IBD - adiponectin, resistin, retinol binding protein 4 (RBP-4), adipocyte fatty acid binding protein and nesfatin-1 in children with IBD according to the presence of 25-hydroxyvitamin D (25(OH)D) deficiency. Methods: The study was conducted as a case-control study in pediatric patients with IBD and healthy children of the same sex and age. In addition to adipokines and 25(OH)D, anthropometric parameters, markers of inflammation and disease activity were assessed in all participants. Results: Children with IBD had significantly higher resistin levels regardless of 25(OH)D levels. IBD patients with 25(OH)D deficiency only had significantly lower RBP-4 compared to healthy controls and also compared to IBD patients without 25(OH)D deficiency. No other significant differences in adipokines were found in children with IBD with or without 25(OH)D deficiency. 25(OH)D levels in IBD patients corelated with RBP-4 only, and did not correlate with other adipokines. Conclusions: Whether the lower RBP-4 levels in the 25(OH)D-deficient group of IBD patients directly reflect vitamin D deficiency remains uncertain. The production of other adipokines does not appear to be directly related to vitamin D deficiency. [ABSTRACT FROM AUTHOR]

Abstract Background Adipose tissue is significantly involved in inflammatory bowel disease (IBD). Vitamin D can affect both adipogenesis and inflammation. The aim of this study was to compare the production of selected adipokines, potentially involved in the pathogenesis of IBD - adiponectin, resistin, retinol binding protein 4 (RBP-4), adipocyte fatty acid binding protein and nesfatin-1 in children with IBD according to the presence of 25-hydroxyvitamin D (25(OH)D) deficiency. Methods The study was conducted as a case-control study in pediatric patients with IBD and healthy children of the same sex and age. In addition to adipokines and 25(OH)D, anthropometric parameters, markers of inflammation and disease activity were assessed in all participants. Results Children with IBD had significantly higher resistin levels regardless of 25(OH)D levels. IBD patients with 25(OH)D deficiency only had significantly lower RBP-4 compared to healthy controls and also compared to IBD patients without 25(OH)D deficiency. No other significant differences in adipokines were found in children with IBD with or without 25(OH)D deficiency. 25(OH)D levels in IBD patients corelated with RBP-4 only, and did not correlate with other adipokines. Conclusions Whether the lower RBP-4 levels in the 25(OH)D-deficient group of IBD patients directly reflect vitamin D deficiency remains uncertain. The production of other adipokines does not appear to be directly related to vitamin D deficiency.

Obesity, which develops especially in childhood and adolescence, is an important health problem at all ages. Hormones that stimulate the hypothalamus about the body's energy stores prevent eating and keep body weight within certain physiological limits. Investigating obesity and the hormones associated with obesity is very important in this context. We believe that the functions of obesity-associated hormones that have been identified to date can guide further studies. In this review, obesity-related hormones and their mechanisms of action are discussed.

Background and Objectives: Inactivity can reduce the serum level of some markers such as nesfatin-1 and irisin, which have positive effects on reducing inflammation and insulin resistance. Thyme is a plant whose extract has various properties, including anti- inflammatory effects. Therefore, the purpose of this research was to investigate the effect of eight weeks of high-intensity interval training (HIIT) along with thyme supplementation on the serum levels of irisin and nesfatin-1 in sedentary young girls Materials and Methods: In this quasi-experimental study, 48 young girls were randomly divided into four groups of HIIT, thyme, HIIT+thyme, and control group. Thyme supplement was taken in the form of 20 mg soft capsules, half an hour before each meal. Serum levels of nesfatin-1 and irisin were analyzed using specific ELISA kits. Data were analyzed using ANOVA and paired t statistical tests with a significance level of 0.05. Results: The serum level of irisin before the test (p=0.685) and after the test (p=0.556) was not significantly different among the studied groups. The post-test values of nesfatin-1 were significantly different among the groups (p<0.001). Intra-group evaluation showed that the changes of nesfatin-1 in the control and thyme groups were not significant (p>0.05). However, a significant increase in nesfatin-1 was observed in HIIT (p<0.001) and HIIT + thyme groups (p=0.001) after the interventions. Conclusion: The increase of nesfatin-1 was one of the favorable effects of HIIT exercises with or without thyme consumption. Irisin levels were not affected by exercise or thyme supplementation. [ABSTRACT FROM AUTHOR]

Background/aim: Our recent study revealed that the expression of lipoxygenase (LOX) and cyclooxygenase (COX) enzymes in the hypothalamus is activated by nesfatin-1, leading to the liberation of leukotrienes and prostaglandins (PG), respectively. Moreover, our prior report explained that intracerebroventricular (ICV) nesfatin-1 treatment triggers cardiovascular responses mediated by central LOX and COX enzymes. Building upon our prior reports, the present investigation sought to clarify the role of cardiovascularly active central COX products, such as thromboxane (TX) A2, PGF2α, PGE, and PGD, in orchestrating nesfatin-1-evoked reactions in mean arterial pressure (MAP) and heart rate (HR). Materials and methods: The Sprague Dawley rats, which had guide cannula in the lateral ventricle for intracerebroventricular (ICV) injections and catheter in arteria femoralis for monitoring MAP and HR, were underwent central pretreatment with furegrelate (the TXA2 synthase inhibitor), PGF2α-dimethylamine (PGF2α-DA, the PGF2α receptor antagonist), or AH6809 (the PGE and PGD receptor antagonist), 5 min prior to ICV nesfatin-1 administration. The cardiovascular parameters were observed and recorded for 60 min posttreatment Results: Nesfatin-1 induced cardiovascular responses in rats leading to pressor effect in MAP, and tachycardia following bradycardia in HR. Interestingly, ICV furegrelate, PGF2α-DA, or AH6809 pretreatment partially mitigated the cardiovascular effects revealed by nesfatin-1. Conclusion: The findings illuminate the role of nesfatin-1 in modulating MAP and HR through the central activation of specifically TXA2, PGF2α, PGE, and PGD from COX metabolites. Additionally, the study may also suggest the potential involvement of other central COX or LOX metabolites beyond these COX metabolites in mediating the cardiovascular effects produced by nesfatin-1. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the influence of abnormal body weight on inflammatory markers and adipokine levels across varied body mass index (BMI) categories. The cohort included 46 participants categorized into normal BMI (group I; n = 19), overweight (group II; n = 14), and obesity (group III; n = 13). Inflammatory markers (hsCRP and IL-6) and adipokines (Adiponectin, Leptin, Nesfatin-1, and Zinc-α2-glycoprotein) were assessed to discern effective indicators of inflammation in individuals with abnormal body weight. Additionally, the full lipid profile was also assessed (total cholesterol, triglycerides, LDL-C, HDL-C). The results indicated significant biochemical changes, particularly in IL-6 and Leptin levels, in participants with a BMI over 25. The levels of ZAG protein were negatively correlated with the HDL-C and LDC-L levels with statistical significance (Pearson: −0.57, p = 0.001, and Pearson: −0.41, p = 0.029, for HDL-C and LDL-C, respectively), suggesting that the level of ZAG is also inversely proportional to the amount of cholesterol. Statistical analyses revealed decreased Zinc-α2-glycoprotein (ZAG) levels and increased Adiponectin, Leptin, and IL-6 levels in individuals with abnormal body weight. Correlation analyses demonstrated a statistically significant upward trend for IL-6 (p = 0.0008) and Leptin (p = 0.00001), with a similar trend observed for hsCRP without statistical significance (p = 0.113). IL-6 levels in the overweight group were 158.71% higher than in the normal-weight group, while the obese group exhibited a 229.55% increase compared to the normal-weight group. No notable changes have been recorded for the levels of Nesfatin-1. Based on our results, we propose IL-6, Leptin, and ZAG as potential biomarkers for monitoring interventions and assessing patient conditions in those with abnormal BMIs. Further research with a larger patient cohort is warranted to validate these correlations in overweight and obese individuals. [ABSTRACT FROM AUTHOR]

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Bronchopulmonary dysplasia (BPD) is a chronic respiratory disease in newborns, which severely influences the health of infants and lacks effective clinical treatment strategies. The pathogenesis of BPD is correlated to enhanced inflammation and activated oxidative stress (OS). The application of antioxidants and antiinflammatory treatment could be hot spots for BPD treatment. Nesfatin-1, a peptide with a suppressive property against inflammation, was tested herein for its potential therapeutic value in BPD. Neonatal SD rats were stimulated with hyperoxia, followed by being intraperitoneally administered with 20 µg/kg/day Nesfatin-1 for 2 weeks. Decreased RAC value in lung tissues, increased wet weight/dry weight (W/D) pulmonary ratio and bronchoalveolar lavage fluid (BALF) proteins, elevated cytokine release in BALF, increased malondialdehyde (MDA) content, and declined superoxide dismutase (SOD) activity were observed in BPD rats, all of which were sharply mitigated by Nesfatin-1. Rat epithelial type II cells (AECIIs) were handled with hyperoxia, and then cultured with 1 and 10 nM Nesfatin-1. Reduced cell viability, elevated lactate dehydrogenase production, elevated cytokine secretion, elevated MDA content, and decreased SOD activity were observed in hyperoxia-handled AECIIs, all of which were markedly alleviated by Nesfatin-1. Furthermore, activated nuclear factor-&#954'B (NF-&#954'B) signaling observed in both BPD rats and hyperoxia-handled AECIIs were notably repressed by Nesfatin-1. Collectively, Nesfatin-1 alleviated hyperoxia-triggered BPD by repressing inflammation and OS via the NF-&#954'B signaling pathway. [ABSTRACT FROM AUTHOR]

ABSTRACT: The study aimed to investigate the distribution and expression of nesfatin-1 in Bactrian camels and its impact on adipocyte glucose metabolism. Polyclonal antibodies against a single antigenic epitope of NUCB2/nesfatin-1 protein were prepared. Nesfatin-1 expression was detected in various adipose tissues, including the hypothalamus, humps, stomach, duodenum, jejunum, ileum, cecum, colon, rectum, pancreas, liver, and abdomen, using Western blot and qRT-PCR. Glucose uptake levels, pyruvic acid content, and hexokinase and phosphofructokinase activities were measured in cultured 3T3-L1 preadipocytes treated with nesfatin-1 in a high glucose state using a non-radiofluorimetric assay. The results showed that nesfatin-1 was found in all Bactrian camel tissues, with higher adipose tissue and pancreas expression. However, qRT-PCR analysis revealed higher expression of nesfatin-1 mRNA in the abdominal fat and liver. After nesfatin-1 treatment, a significant decrease (p

Objective: This study aims to explore the impact of Nesfatin-1 on type 2 diabetic erectile dysfunction (T2DMED) and its underlying mechanism in regulating the phenotypic switching of corpus cavernosum smooth muscle cells (CCSMCs). Methods: Twenty-four 4-week-old male C57 wild-type mice were randomly assigned to the control group, model group, and Nesfatin-1 treatment group. Monitoring included body weight, blood glucose levels, and penile cavernous pressure (ICP). Histochemistry and Western blot analyses were conducted to assess the expressions of α-SMA, OPN, and factors related to the PI3K/AKT/mTOR signaling pathway. CCSMCs were categorized into the control group, high glucose and high oleic acid group (GO group), Nesfatin-1 treatment group (GO + N group), sildenafil positive control group (GO + S group), and PI3K inhibitor group (GO + N + E group). Changes in phenotypic markers, cell morphology, and the PI3K/AKT/mTOR signaling pathway were observed in each group. Results: (1) Nesfatin-1 significantly ameliorated the body size, body weight, blood glucose, glucose tolerance, and insulin resistance in T2DMED mice. (2) Following Nesfatin-1 treatment, the ICP/MSBP ratio and the peak of the ICP curve demonstrated a significant increase. (3) Nesfatin-1 significantly enhanced smooth muscle and reduced collagen fibers in the corpus cavernosum. (4) Nesfatin-1 notably increased α-SMA expression and decreased OPN expression in CCSMCs. (5) Nesfatin-1 elevated PI3K, p-AKT/AKT, and p-mTOR/mTOR levels in penile cavernous tissue. Conclusions: Nesfatin-1 not only effectively improves body weight and blood glucose levels in diabetic mice but also enhances erectile function and regulates the phenotypic switching of corpus cavernosum smooth muscle. The potential mechanism involves Nesfatin-1 activating the PI3K/AKT/mTOR signaling pathway to induce the conversion of CCSMCs to a contractile phenotype.

Background and Aims: Adipokines omentin-1 and nesfatin-1 are hormones secreted from adipose tissue that effectively regulate metabolic pathways. On the other hand, exercise training plays a positive role in preventing metabolic diseases. The present study aimed to investigate the effect of aerobic and resistance training on the levels of omentin-1 and nesfatin-1 in adults. Materials and Methods: A systematic search of English and Persian articles published in PubMed, Web of Science, SID, Scopus, and Magiran databases was conducted until September 2023. A meta-analysis was conducted to investigate the effect of aerobic and resistance training on the levels of omentin-1 and nesfatin-1 in adults. The mMean difference and 95% confidence interval (CI) were calculated using a random effect model. Heterogeneity was evaluated using the I2 test, and diffusion bias was evaluated by visual analysis of the funnel plot and Egger's test. Results: In total, 26 studies, including 29 exercise interventions and 722 adults, 409 participants in the exercise group with an average age of 32.45 ± 3.71, and 313 participants in the control group with an average age of 29.86 ± 2.34 were added to the present meta-analysis. The results showed that exercise training caused a significant increase in omentin-1 [SMD=1.37, 0.83 to 1.91, P=0.001] and nesfatin-1 [SMD= 0.69, 0.01 to 1.37, P=0.04] compared to the control group in adults. Conclusion: The results of the present study showed that both types of aerobic and resistance training lead to a significant increase in the levels of omentin-1 and nesfatin-1. It seems that exercise training can be a non-pharmacological and practical intervention to regulate adipokines in adults.

Abstract Nucleobindin-derived peptides, nesfatin-1 [NESF-1] and nesfatin-1-like-peptide [NLP] have diverse roles in endocrine and metabolic regulation. While both peptides showed a stimulatory effect on the synthesis of proopiomelanocortin (POMC), the adrenocorticotropic hormone (ACTH) precursor in mouse corticotrophs, whether NESF-1 and NLP have any direct effect on glucocorticoid [GC] synthesis in the adrenal cortex remains unknown. The main aim of this study was to determine if NESF-1 and/or NLP act directly on adrenal cortex cells to regulate cortisol synthesis in vitro. Whether NLP injection affects stress-hormone gene expression in the adrenal gland and pituitary in vivo in mice was also assessed. In addition, cortisol synthetic pathway in Nucb1 knockout mice was studied. Human adrenal cortical [H295R] cells showed immunoreactivity for both NUCB1/NLP and NUCB2/NESF-1. NLP and NESF-1 decreased the abundance of steroidogenic enzyme mRNAs, and cortisol synthesis and release through the AC/PKA/CREB pathway in H295R cells. Similarly, intraperitoneal injection of NLP in mice decreased the expression of enzymes involved in glucocorticoid (GC) synthesis in the adrenal gland while increasing the expression of Pomc, Pcsk1 and Crhr1 in the pituitary. Moreover, the melanocortin 2 receptor (Mc2r) mRNA level was enhanced in the adrenal gland samples of NLP injected mice. However, the global genetic disruption in Nucb1 did not affect most steroidogenic enzyme mRNAs, and Pomc, Pcsk2 and Crhr1 mRNAs in mice adrenal gland and pituitary gland, respectively. Collectively, these data provide the first evidence for a direct inhibition of cortisol synthesis and secretion by NLP and NESF-1. NUCB peptides might still elicit a net stimulatory effect on GC synthesis and secretion through their positive effects on ACTH-MC2R pathway in the pituitary.

The prevalence of osteoporosis has been on the rise globally. With ageing populations, research has sought therapeutic solutions in novel areas. One such area is that of the adipokines. Current literature points to an important role for these chemical mediators in relation to bone metabolism. Wellestablished adipokines have been broadly reported upon. These include adiponectin and leptin. However, other novel adipokines such as visfatin, nesfatin-1, meteorin-like protein (Metrnl), apelin and lipocalin-2 are starting to be addressed pre-clinically and clinically. Adipokines hold pro-inflammatory and anti-inflammatory properties that influence the pathophysiology of various bone diseases. Omentin-1 and vaspin, two novel adipokines, share cardioprotective effects and play essential roles in bone metabolism. Studies have reported boneprotective effects of omentin-1, whilst others report negative associations between omentin-1 and bone mineral density. Lipocalin-2 is linked to poor bone microarchitecture in mice and is even suggested to mediate osteoporosis development from prolonged disuse. Nesfatin-1, an anorexigenic adipokine, has been known to preserve bone density. Animal studies have demonstrated that nesfatin-1 treatment limits bone loss and increases bone strength, suggesting exogenous use as a potential treatment for osteopenic disorders. Pre-clinical studies have shown adipokine apelin to have a role in bone metabolism, mediated by the enhancement of osteoblast genesis and the inhibition of programmed cell death. Although many investigations have reported conflicting findings, sufficient literature supports the notion that adipokines have a significant influence on the metabolism of bone. This review aims at highlighting the role of novel adipokines in osteoporosis while also discussing their potential for treating osteoporosis. [ABSTRACT FROM AUTHOR]

Boron (B) is an element that has recently been wondered and researched in many fields, especially due to its effects on energy metabolism. The aim of this study is to evaluate the effect of boric acid (BA) on newly discovered energy metabolism peptides that have not been studied before. In this study, the effects of 15 mg/kg of BA were evaluated in 24 Wistar rats. Groups were named as control group, 15 mg/kg BA group, streptozotocin (STZ)-induced experimental diabetic group, and STZ-induced experimental diabetic + 15 mg/kg BA administered group (STZ+15 mg/kg BA). Serum asprosin, nesfatin-1, preptin, insulin, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), aspartate transaminase (AST), alanine transaminase (ALT), and glucose analyses were performed. In this study, the increase in glucose, TG, TC, LDL-C levels, and AST, ALT activities in STZ-induced groups were reduced with BA administration. While HDL-C level significantly decreased in the STZ group, the level approached the control group values after BA administration (p<0.001). As for peptides, although there was a statistically significant increase after 15 mg/kg BA administration, these levels did not approach the control group values (p<0.001). According to the findings, STZ-induced diabetes mellitus and the biochemical processes that develop accordingly change correlatively. This study showed that BA is effective in energy metabolism. [ABSTRACT FROM AUTHOR]

Nucleobindin-derived peptides, nesfatin-1 [NESF-1] and nesfatin-1-like-peptide [NLP] have diverse roles in endocrine and metabolic regulation. While both peptides showed a stimulatory effect on the synthesis of proopiomelanocortin (POMC), the adrenocorticotropic hormone (ACTH) precursor in mouse corticotrophs, whether NESF-1 and NLP have any direct effect on glucocorticoid [GC] synthesis in the adrenal cortex remains unknown. The main aim of this study was to determine if NESF-1 and/or NLP act directly on adrenal cortex cells to regulate cortisol synthesis in vitro. Whether NLP injection affects stress-hormone gene expression in the adrenal gland and pituitary in vivo in mice was also assessed. In addition, cortisol synthetic pathway in Nucb1 knockout mice was studied. Human adrenal cortical [H295R] cells showed immunoreactivity for both NUCB1/NLP and NUCB2/NESF-1. NLP and NESF-1 decreased the abundance of steroidogenic enzyme mRNAs, and cortisol synthesis and release through the AC/PKA/CREB pathway in H295R cells. Similarly, intraperitoneal injection of NLP in mice decreased the expression of enzymes involved in glucocorticoid (GC) synthesis in the adrenal gland while increasing the expression of Pomc, Pcsk1 and Crhr1 in the pituitary. Moreover, the melanocortin 2 receptor (Mc2r) mRNA level was enhanced in the adrenal gland samples of NLP injected mice. However, the global genetic disruption in Nucb1 did not affect most steroidogenic enzyme mRNAs, and Pomc, Pcsk2 and Crhr1 mRNAs in mice adrenal gland and pituitary gland, respectively. Collectively, these data provide the first evidence for a direct inhibition of cortisol synthesis and secretion by NLP and NESF-1. NUCB peptides might still elicit a net stimulatory effect on GC synthesis and secretion through their positive effects on ACTH-MC2R pathway in the pituitary. [ABSTRACT FROM AUTHOR]

Simple Summary: Aggression stands out as one of the most prevalent behavior problems in dogs, with a particular predisposition noted in Pit Bull breeds. To advance our understanding and develop new treatment strategies for aggression, it is crucial to explore the neurobiological foundations of this behavior. In our study, Pit Bull dogs were categorized based on aggression levels through the administration of aggression tests. Plasma nesfatin-1, serotonin, dopamine, and oxytocin levels were determined in blood samples collected after a 24 h fasting period and 2 h after refeeding. The results, a pioneering contribution to the literature, indicate a novel association between decreased plasma levels of nesfatin-1, serotonin, and oxytocin and increased dopamine levels with aggression in Pit Bull dogs. During fasting conditions, lower plasma levels of nesfatin-1, serotonin, and dopamine were observed, while plasma oxytocin levels were higher. Our findings underscore the significant roles of nesfatin-1, serotonin, oxytocin, and dopamine in the aggression of Pit Bull dogs, revealing potential interactions among these neuropeptides at the central nervous system level. Aggression is a prevalent and concerning behavioral issue in dogs. Pit Bull dogs, known for their high levels of aggression, are recognized as a focus of concern in society. In our study, we aimed to investigate the behavioral characteristics of Pit Bull dogs and explore the potential roles of peptides involved in the neurobiology of aggression. Initially, female, and male dogs underwent aggression tests, and their aggression levels were categorized. Plasma nesfatin-1, serotonin, oxytocin, and dopamine levels were quantified using ELISA, with blood samples collected after a 24 h fasting period and 2 h post-refeeding. Our findings indicate that aggression in Pit Bull dogs correlates with decreased plasma nesfatin-1, serotonin, and oxytocin levels, while dopamine levels increase. The study's findings indicate that fasted dogs exhibited lower plasma levels of nesfatin-1, serotonin, and dopamine, while plasma oxytocin levels were higher. Furthermore, while the research findings do not suggest a significant relationship between the severity of aggression and the gender of the dog, male Pit Bull breeds appear to have higher plasma nesfatin-1 and serotonin levels compared to their female counterparts. The study's findings demonstrate that nesfatin-1, serotonin, oxytocin, and dopamine play pivotal roles in Pit Bull dogs' aggression, indicating potential interactions among these neuropeptides at the central nervous system level. [ABSTRACT FROM AUTHOR]

Background: Previous studies have investigated the relationship between nesfatin-1 level and polycystic ovary syndrome (PCOS). However, these studies have produced conflicting results. Thus, in this meta-analysis, we aimed to clarify the association between blood nesfatin-1 levels and PCOS, and the ability of nesfatin-1 as a biomarker in PCOS. Methods: Meta-analysis was performed using STATA 12.0 software. We computed standard mean difference (SMD) and 95% confidence interval (CI) regarding the comparison of blood nesfatin-1 in patients with PCOS and controls. Results: The present meta-analysis showed no significant difference in blood nesfatin-1 level between patients with PCOS and controls with a random effects model (SMD = 0.03; 95%CI: -0.71, 0.77; I² = 97.1%, p value for Q test < 0.001). Subgroup analysis for different ethnicities reported no significant difference in blood nesfatin-1 level between patients with PCOS and controls in both Caucasian and Asian populations. Subgroup analysis for different sample types reported no significant difference in serum nesfatin-1 level between patients with PCOS and controls. Subgroup studies reported no significant difference in blood nesfatin-1 level between PCOS and controls in both obese and non- obese populations. Conclusion: In conclusion, there is no significant relationship between blood nesfatin-1 levels and PCOS. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the effect of cinnamaldehyde (CA) on fasting blood glucose (FBG), body weight, lipid profile, and nesfatin-1 levels in healthy and diabetic (DM) rats. Methods: Ten groups with eight rats per group were used. Healthy and diabetic sham groups were administered 1 mL of saline for 28 days by intragastric gavage. Healthy and diabetic control groups were administered 1 mL 0.5 % dimethyl sulfoxide (DMSO) for 28 days by intragastric gavage. Other diabetic and healthy groups (HG) received 10, 20, and 40 mg/kg CA for 28 days by intragastric gavage, once daily. Diabetes was induced with streptozotocin (50 mg/kg intraperitoneally). Rats were defined as diabetic when FBG was > 250 mg/dL. Enzyme-linked immunosorbent assay (ELISA) was used to assess serum nesfatin-1 concentrations. Fasting blood glucose (FBG) values were evaluated with a glucometer. Results: Day 28 weights of all DM and HG + 40 mg/kg CA groups were lower than day 1 weights (p < 0.05). Triglyceride values of DM + 40 mg/kg CA group were lower than DM sham and control group (p = 0.001). Low-density lipoprotein (LDL) and cholesterol levels of the CA-administered healthy groups were higher than healthy control groups (p = 0.001). Nesfatin-1 levels of all DM groups were lower than all healthy groups, and nesfatin-1 levels of all CA-administered healthy and DM groups were lower than healthy and DM sham and control groups, but these were not significant (p > 0.001). Conclusion: Although not significant, the decrease in nesfatin-1 level is evidence that CA has an antiobesity effect in both healthy and diabetic rats. In contrast to its antihyperlipidemic effect in diabetic conditions, CA has hyperlipidemic effect in healthy conditions. [ABSTRACT FROM AUTHOR]

Background and Objectives: The NUCB2 gene and its polymorphisms were identified as novel players in the regulation of food intake, potentially leading to obesity (OBE) and altered eating behaviors. Naltrexone/bupropion SR (NB) showed good efficacy and tolerability for treating OBE and altered eating behaviors associated with binge eating disorder (BED). This prospective study investigates the influence of NUCB2 gene polymorphism on NB treatment response in OBE and BED. Materials and Methods: Body mass index (BMI), eating (EDE-Q, BES, NEQ, GQ, Y-FAS 2.0) and general psychopathology (BDI, STAI-S) were evaluated at baseline (t0) and after 16 weeks (t1) of NB treatment in patients with OBE and BED (Group 1; N = 22) vs. patients with OBE without BED (Group 2; N = 20). Differences were evaluated according to the rs757081 NUCB2 gene polymorphism. Results: NUCB2 polymorphism was equally distributed between groups. Although weight at t0 was higher in Group 1, weight loss was similar at t1 in both groups. BMI was not influenced by NUCB2 polymorphism. In Group 1, the CG-genotype reported significant improvement in eating psychopathology while the GG-genotype reported improvement only for FA. No differences were observed in Group 2. Conclusions: Patients diagnosed with BED and treated with NB exhibited a more favorable treatment response within the CG-genotype of the NUCB2 polymorphism. [ABSTRACT FROM AUTHOR]

Normal gonadal function can be disrupted by hypothyroidism. Hypothyroidism disturbs testicular function directly and centrally by affecting the hypothalamic‐pituitary‐testicular axis with unclear mechanism. As nesfatin‐1 neurons co‐localized with TRH and GnRH neurons in the hypothalamus, it could play a role in centrally hypothyroidism induced testicular dysfunction. Selenium (Se), by affecting thyroid iodide supply, could relieve these disturbances. So, we aim to identify the role of nesfatin‐1 as a link between testicular dysfunction and hypothyroidism through modulating the MAPK/ERK pathway while discussing the possible role of Se in alleviating hypothyroidism and associated testicular damage. Forty male rats were divided equally into: Control: distilled water, Se: Se orally, Propylthiouracil (PTU): PTU orally, PTU + Se: Se with PTU orally. Serum thyroid function, gonadal hormones, nesfatin‐1, testicular redox status, sperm analysis, brain tissue GnRH, nucleobindin 2‐derived polypeptide, pMAPK/ERK gene expression, histological changes and immunohistochemical expression of testicular proliferating cell antigen (PCNA) were done. PTU induced hypothyroidism and reduction of gonadal hormones which both were correlated with reduced nesfatin‐1. There was testicular stress with reduced GnRH, NUCB2, pMAPK/ERK gene expression, and PCNA immunopositive cells. These parameters were reversed by Se. Nesfatin‐1 could be the central link between hypothyroidism and disturbances of the hypothalamic pituitary testicular axis. [ABSTRACT FROM AUTHOR]

Nesfatin-1 is a novel adipocytokine consisting of 82 amino acids with anorexic and anti-hyperglycemic properties. Further studies of nesfatin-1 have shown it to be closely associated with neurological disorders. Changes in nesfatin-1 levels are closely linked to the onset, progression and severity of neurological disorders. Nesfatin-1 may affect the development of neurological disorders and can indicate disease evolution and prognosis, thus informing the choice of treatment options. In addition, regulation of the expression or level of nesfatin-1 can improve the level of neuroinflammation, apoptosis, oxidative damage and other indicators. It is demonstrated that nesfatin-1 is involved in neuroprotection and may be a therapeutic target for neurological disorders. In this paper, we will also discuss the role of nesfatin-1 as a biomarker in neurological diseases and its potential mechanism of action in neurological diseases, providing new ideas for the diagnosis and treatment of neurological diseases. [ABSTRACT FROM AUTHOR]

Copyright of Ahi Evran Medical Journal is the property of Ahi Evran University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

There are some initial suggestions in the literature that phoenixin, spexin, nesfatin-1 and kisspeptin may play a role in the pathogenesis of affective disorders. Therefore, they may also be cautiously considered as potential diagnostic or predictive biomarkers of BD. This study aimed to evaluate the levels of the aforementioned neuropeptides in the peripheral blood of children and adolescents with bipolar. This study included 122 individuals: 67 persons with diagnosed bipolar disorder types I and II constituted the study group, and 55 healthy persons were included in the control group. Statistically significant differences in the concentrations of neuropeptides between the control and study groups were noted in relation to nesfatin-1 and spexin (although spexin lost statistical significance after introducing the Bonferroni correction). In a logistic regression analysis, an increased risk of bipolar disorder was noted for a decrease in nesfatin-1 concentration. Lower levels of nesfatin-1 seemed to be a significant risk factor for the development of bipolar disorder types I and II. Furthermore, the occurrence of bipolar disorder was associated with significantly elevated levels of spexin. None of the analyzed neuropeptides was significantly correlated with the number of symptoms of bipolar disorder. [ABSTRACT FROM AUTHOR]

Copyright of Baghdad Science Journal is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The physiological process of birth can cause stress in animals because it affects many mechanisms. The aim of this study was to determine the effect of the type of birth on the Nesfatin–1 level and to explain the relationship with oxidative stress parameters in Awassi breed sheep. The study included a total of 60 sheep with a singleton birth in 3 groups: as Group 1 (n:20) including animals that had a normal birth, Group 2 (n:20) that had a difficult birth (dystocia), and Group 3 (n:20) including sheep that gave birth by caesarean section. Blood samples were taken from the sheep in all the groups within 10 min of the birth, for the measurement of Nesfatin–1, total antioxidant capacity (TAS), and total oxidant capacity (TOS). The data obtained were examined with One–Way Variance Analysis, and relationships between the data with the Pearson test. Statistically significant differences were determined between the groups in respect of Nesfatin–1, TAS, TOS, and oxidative stress index (OSI) levels (P

There are many studies on nesfatin-1, omentin, adropin, leptin, and ghrelin. However, data on the effects of long, medium, and short chain fatty acids on serum/tissue concentrations of nesfatin-1, omentin, adropin, leptin, and ghrelin are scarce. This study aims to investigate the effects of butyric acid, caprylic acid, and oleic acid alone or in combination on nesfatin-1, omentin, adropin, leptin, and ghrelin secretion. In the study, 49 male Wistar rats were used. The rats were randomly divided into 7 groups as control (CONT), butyric acid (BA), caprylic acid (CA), oleic acid (OA), butyric acid+caprylic acid (BA+CA), butyric acid+oleic acid (BA+OA) and caprylic acid+oleic acid (CA+OA) groups. The rats were orally administered fatty acids for twenty-one days. At the end of the study, the levels of nesfatin-1, omentin, adropin, leptin, and ghrelin were determined by the ELISA method. When the groups were compared in terms of nesfatin-1, omentin, adropin, leptin, and ghrelin levels, the butyric acid group had higher nesfatin-1, omentin, adropin, leptin, and ghrelin levels than the other groups (p0.05). In conclusion, it was observed that butyric acid use caused an increase in serum nesfatin-1, omentin, adropin, leptin, and ghrelin levels. [Med-Science 2023; 12(4.000): 1117-23]

AIM:To analyze the correlation between serum nesfatin-1, apelin and heme oxygenase-1(HO-1)levels and the severity of diabetic retinopathy(DR).METHODS:Totally 100 patients with type 2 diabetes mellitus(T2DM)who were admitted to the hospital from September 2020 to September 2022 were selected. They were divided into non-DR(NDR)group(35 cases), nonproliferative DR(NPDR)group(33 cases)and proliferative DR(PDR)group(32 cases)according to the condition of fundus lesions. Another 30 healthy individuals who received health check-ups in the hospital during the same period were selected as the control group. Serum nesfatin-1, apelin and HO-1 levels in each group were detected, and panretinal ischemia index(ISI)was evaluated.RESULTS:Serum nesfatin-1 and HO-1 levels in the T2DM patients were lower, and apelin level was higher as compared with the control group. The levels of nesfatin-1 and HO-1 in the PDR group were the lowest, while the apelin level was the highest. Panretinal ISI in the PDR group was higher than that in the NPDR group(4.56±0.57 vs. 2.05±0.29, P

Nesfatin-1, deriving from a precursor protein, NUCB2, is a newly discovered molecule with anti-apoptotic, anti-inflammatory, antioxidant, and anorexigenic effects. It was initially identified in the central nervous system (CNS) and received increasing interest due to its energy-regulating properties. However, research showed that nesfatin-1 is also expressed in peripheral tissues, including the digestive system. The aim of this review is to give a résumé of the present state of knowledge regarding its structure, immunolocalization, and potential implications in diseases with inflammatory components. The main objective was to focus on its clinical importance as a diagnostic biomarker and potential therapeutic molecule in a variety of disorders, among which digestive disorders were of particular interest. Previous studies have shown that nesfatin-1 regulates the balance between pro- and antioxidant agents, which makes nesfatin-1 a promising therapeutic agent. Further in-depth research regarding the underlying mechanisms of action is needed for a better understanding of its effects.

The aim of this rapid review is to examine the research evidence that presents the effects of physical activity and exercise on Nucleobindin‐2 (NUCB2) gene expression and Nesfatin‐1 concentration. Five databases (PubMed, Science Direct, Springer, Wiley, and Google Scholar) were searched for eligible studies from the earliest available date to August 2023. In human studies, Nesfatin‐1 concentration either remains unchanged or increases after exercise training. It appears that higher exercise intensity and longer duration of training accentuate the increase of blood Nesfatin‐1 concentration. The few human studies that have examined the acute response of exercise on Nesfatin‐1 concentration from blood draws show conflicting results. There is a severe lack of biopsy studies in humans which warrants attention. All published animal studies have used the mouse model. The majority show that regular exercise training increases tissue NUCB2/Nesfatin‐1. In some animal studies, where the effects of exercise on tissue Nesfatin‐1 concentration has been seen as significant, there has been no significant effect of exercise on plasma Nesfatin‐1 concentration. All animal studies evaluated the effect of endurance training except one which used resistance training. No animal studies have investigated the effects of acute exercise, which warrants investigation. In conclusion, human and animal studies have shown that physical training can increase NUCB2/Nesfatin‐1, but research evidence examining the effect of acute exercise is in its infancy. In addition, future comparative studies are needed to compare the effects of different training protocols on NUCB2/Nesfatin‐1 in humans and animals. Significance statement: The purpose of conducting this review is to assess the existing research evidence regarding the impact of exercise on Nucleobindin‐2 (NUCB2) gene expression and Nesfatin‐1 concentration. It is worth noting that, to the best of our knowledge, no previous review article has been published on this specific topic. Therefore, the objective of this review is to provide a comprehensive overview for the first time, focusing on the influence of exercise on Nesfatin‐1/NUCB2. In addition, this review will also identify any research gaps and provide valuable recommendations for future studies. It is hoped that these recommendations will inspire further research in this field, ultimately enhancing our understanding of the effects of exercise on neuropeptides and their implications for appetite and energy balance. [ABSTRACT FROM AUTHOR]

There are many studies on nesfatin-1, omentin, adropin, leptin, and ghrelin. However, data on the effects of long, medium, and short chain fatty acids on serum/tissue concentrations of nesfatin-1, omentin, adropin, leptin, and ghrelin are scarce. This study aims to investigate the effects of butyric acid, caprylic acid, and oleic acid alone or in combination on nesfatin-1, omentin, adropin, leptin, and ghrelin secretion. In the study, 49 male Wistar rats were used. The rats were randomly divided into 7 groups as control (CONT), butyric acid (BA), caprylic acid (CA), oleic acid (OA), butyric acid+caprylic acid (BA+CA), butyric acid+oleic acid (BA+OA) and caprylic acid+oleic acid (CA+OA) groups. The rats were orally administered fatty acids for twenty-one days. At the end of the study, the levels of nesfatin-1, omentin, adropin, leptin, and ghrelin were determined by the ELISA method. When the groups were compared in terms of nesfatin-1, omentin, adropin, leptin, and ghrelin levels, the butyric acid group had higher nesfatin-1, omentin, adropin, leptin, and ghrelin levels than the other groups (p<0.05). No statistically significant difference was found in the other groups (p>0.05). In conclusion, it was observed that butyric acid use caused an increase in serum nesfatin-1, omentin, adropin, leptin, and ghrelin levels. [ABSTRACT FROM AUTHOR]

Background/aim: Due to the increasing mortality and morbidity rates in diabetes mellitus (DM), which is one of the biggest health problems of our age, many treatment modalities are still being tried. The positive effects of metformin (MET) and physical exercise (EXE) on the pathophysiology of diabetes are well known. In this study, it was aimed to detail these positive effects of MET and EXE in combination on the basis of inflammation, apoptosis mechanisms, and endogen nesfatin-1 (NES-1) synthesis. Materials and methods: Twenty-seven type 2 DM (DM-2) male Wistar Albino rats were divided into 4 groups, as the high-fat diet (HFD), MET, EXE, and MET+EXE groups. The total duration of the study was 3 months. At the end of the experiment, blood glucose and lipid profiles were measured. Histopathological evaluation was performed on the cardiac and aortic tissues and apoptotic markers were evaluated immunohistochemically. Inflammatory markers and NES-1 levels were analyzed by enzyme-linked immunosorbent assay. Results: The plasma glucose, homeostatic model evaluation-insulin resistance (HOMA-IR), low-density lipoprotein (LDL) levels increased, and high-density lipoprotein (HDL) levels decreased significantly in the HFD group. In the treatment groups, the glucose, HOMA-IR, LDL, NES-1 levels in the plasma, as well as tumor necrosis factor alpha (TNF-a), interleukin-1 beta (IL-1ß), IL-6, caspase-3 (Cas-3), Bcl-2-associated X protein (Bax), and histopathological findings of inflammation in tissues were decreased. Additionally, there was an increase in plasma insulin, HDL, and tissue B-cell lymphoma-2 and levels. Conclusion: It was observed that the MET and EXE treatments in the DM-2 model reduced cellular damage mechanisms such as inflammation and apoptosis. The decrease in NES-1 levels was thought to be secondary to this antiinflammatory effect. In conclusion, the results demonstrated the effectiveness of EXE in reducing DM-2 and the NES-1 levels. Further studies are needed to evaluate the effect in different EXE models and treatment durations. [ABSTRACT FROM AUTHOR]

Background and Aims: Adipokines omentin-1 and nesfatin-1 are hormones secreted from adipose tissue that effectively regulate metabolic pathways. On the other hand, exercise training plays a positive role in preventing metabolic diseases. The present study aimed to investigate the effect of aerobic and resistance training on the levels of omentin-1 and nesfatin-1 in adults. Materials and Methods: A systematic search of English and Persian articles published in PubMed, Web of Science, SID, Scopus, and Magiran databases was conducted until September 2023. A meta-analysis was conducted to investigate the effect of aerobic and resistance training on the levels of omentin-1 and nesfatin1 in adults. The mMean difference and 95% confidence interval (CI) were calculated using a random effect model. Heterogeneity was evaluated using the I2 test, and diffusion bias was evaluated by visual analysis of the funnel plot and Egger's test. Results: In total, 26 studies, including 29 exercise interventions and 722 adults, 409 participants in the exercise group with an average age of 32.45 ± 3.71, and 313 participants in the control group with an average age of 29.86 ± 2.34 were added to the present meta-analysis. The results showed that exercise training caused a significant increase in omentin-1 [SMD=1.37, 0.83 to 1.91, P=0.001] and nesfatin-1 [SMD= 0.69, 0.01 to 1.37, P=0.04] compared to the control group in adults. Conclusion: The results of the present study showed that both types of aerobic and resistance training lead to a significant increase in the levels of omentin-1 and nesfatin-1. It seems that exercise training can be a nonpharmacological and practical intervention to regulate adipokines in adults. [ABSTRACT FROM AUTHOR]

Purpose: With the increasing prevalence of metabolic disorders, studies on energy metabolism have advanced, leading to the recent identification of new members in energy metabolism. This study aims to demonstrate the effects of a high-calorie diet and exercise on the newly identified peptides asprosin, irisin, nesfatin-1, and preptin, whose effects on metabolism are still under investigation, and to provide information for future research. Materials and Methods: In this study, 24 rats were divided into four groups: control, exercise, high-calorie diet, and high-calorie diet with exercise. Serum levels of asprosin, irisin, preptin, nesfatin-1, and insulin were measured using the ELISA method. Additionally, serum levels of glucose, triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were determined by the colorimetric method. Results: Compared to the control group, there were significant increases in body mass index, glucose, asprosin, TG, TC, and LDL-C levels. Serum HDL-C levels were notably lower in the experimental group compared to the control group. In the exercise group, irisin and nesfatin-1 levels significantly increased, accompanied by reductions in LDL-C, TG, TC, glucose, and preptin levels. Conclusion: A high-calorie diet was associated with an unfavorable lipid profile, while exercise-induced alterations in the secretion of peptides derived from adipose tissue and/or regulating energy metabolism. Although physical activity emerges as a crucial factor in peptide secretion and maintaining biochemical balance, further research is imperative to comprehensively understand the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Background: Recent changes in dietary habits have resulted in increased intake of advanced glycation end products (AGEs), which are known to have a predominant contribution to the pathogenesis and complications of coronary artery disease (CAD). AGEs are also thought to induce weight gain by affecting appetite, energy expenditure, and brown adipose tissue (BAT). Here, we investigated whether the restriction of dietary AGEs could affect appetite, body composition, anthropometric indices, and BAT-derived markers in CAD patients treated with angioplasty. Materials and Methods: Forty-two stented CAD patients were randomly allocated into two groups that received either a low-AGEs or a control diet for 12 weeks. At baseline and postintervention, fasting blood samples were analyzed for total AGEs, nesfatin-1, and BAT-derived markers (fibroblast growth factor 21 and neuregulin 4). Subjective appetite ratings and body composition were evaluated using the Visual Analog Scale (VAS) and bioelectric impedance analysis. Anthropometric indices, including fat mass index (FMI), abdominal volume index (AVI), and body adiposity index (BAI), were calculated through the relevant formula. Results: Restricting dietary AGEs for 12 weeks could cause a significant reduction in weight, FMI, AVI, and BAI (P < 0.05) compared to the comparison group. In addition, VAS data analyses indicated a significant decrease in the sense of hunger and prospective food intake (P < 0.05) in the intervention group compared to the comparison group. No significant difference was seen in the measured biochemical markers between the two groups. Conclusion: This study indicated that the low-AGEs diet could decrease appetite, weight, and anthropometric indices in stented CAD patients. [ABSTRACT FROM AUTHOR]

The prevalence of central precocious puberty (CPP) in girls has increased worldwide and is often associated with obesity in childhood as well as high fat/high glycemic index diets. Evidence suggests that subjects with obesity present with alterations in appetite-regulating hormones. The arcuate and paraventricular nuclei of the hypothalamus are the centers of action of appetite hormones, as well as the location of gonadotropin-releasing hormone (GnRH) neurons, the activation of which results in the onset of puberty. This anatomical proximity raises the question of possible alterations in appetite-regulating hormones in patients with CPP. Furthermore, diet-induced hypothalamic inflammation constitutes a probable mechanism of the pathophysiology of CPP, as well as alterations in appetite-regulating hormones in young children. In this article, we summarize the evidence investigating whether girls with CPP present with alterations in appetite-regulating hormones. We present evidence that leptin concentrations are elevated in girls with CPP, ghrelin concentrations are lower in girls with CPP, nesfatin-1 and orexin-A concentrations are elevated among girls with premature thelarche, and insulin concentrations are increased in girls with early menarche. [ABSTRACT FROM AUTHOR]

Sleep contributes to the energy balance of body. This study aims to investigate how rapid eye movement (REM) sleep deprivation (SD) or recovery sleep affects rat weight and the serum levels of Nesfatin-1, Orexin-A, and Leptin; additionally, seeks to determine the impact of melatonin administration on these parameters. Male, Sprague Dawley rats were randomized into two groups (n=9). REMSD was induced using the modified multiple platform method (MMPM). Melatonin was used as a treatment (20 mg/kg). Study Group I was created to investigate the effectiveness of the treatment during REMSD. Study Group II was established to analyze the possible therapeutic role of melatonin and recovery sleep after REMSD-induced damage. The rats" weights were recorded during the experiments. Blood samples were collected from all rats via decapitation after experiments. The levels of serum Nesfatin-1, Orexin-A, and Leptin were analyzed using the ELISA method. REMSD affected weight of the rats and altered the levels of serum Nesfatin-1 and Leptin. Melatonin administration influenced weight gain and affected Nesfatin-1 and Leptin levels. REMSD or melatonin did not affect Orexin-A levels. REMSD and melatonin play significant roles in the body"s energy balance. This study will contribute to elucidating the role of SD in metabolic processes and will play a role in assessing the impact of melatonin, a commonly used treatment in human and veterinary medicine.

This study aimed to investigate the influence of abnormal body weight on inflammatory markers and adipokine levels across varied body mass index (BMI) categories. The cohort included 46 participants categorized into normal BMI (group I; n = 19), overweight (group II; n = 14), and obesity (group III; n = 13). Inflammatory markers (hsCRP and IL-6) and adipokines (Adiponectin, Leptin, Nesfatin-1, and Zinc-α2-glycoprotein) were assessed to discern effective indicators of inflammation in individuals with abnormal body weight. Additionally, the full lipid profile was also assessed (total cholesterol, triglycerides, LDL-C, HDL-C). The results indicated significant biochemical changes, particularly in IL-6 and Leptin levels, in participants with a BMI over 25. The levels of ZAG protein were negatively correlated with the HDL-C and LDC-L levels with statistical significance (Pearson: −0.57, p = 0.001, and Pearson: −0.41, p = 0.029, for HDL-C and LDL-C, respectively), suggesting that the level of ZAG is also inversely proportional to the amount of cholesterol. Statistical analyses revealed decreased Zinc-α2-glycoprotein (ZAG) levels and increased Adiponectin, Leptin, and IL-6 levels in individuals with abnormal body weight. Correlation analyses demonstrated a statistically significant upward trend for IL-6 (p = 0.0008) and Leptin (p = 0.00001), with a similar trend observed for hsCRP without statistical significance (p = 0.113). IL-6 levels in the overweight group were 158.71% higher than in the normal-weight group, while the obese group exhibited a 229.55% increase compared to the normal-weight group. No notable changes have been recorded for the levels of Nesfatin-1. Based on our results, we propose IL-6, Leptin, and ZAG as potential biomarkers for monitoring interventions and assessing patient conditions in those with abnormal BMIs. Further research with a larger patient cohort is warranted to validate these correlations in overweight and obese individuals.

Objective:This study aims to investigate the expression of Nesfatin-1, Galectin-3, Ghrelin, and Leptin in mediastinal adipose tissue and their relationship with postoperative complications in patients with and without metabolic syndrome who underwent on-pump coronary artery bypass graft (CABG) surgery.Method:Fifty patients who underwent CABG surgery and who were in sinus rhythm were included in the study. The patients were divided into two groups according to whether they had metabolic syndrome or not. All patients’ age, gender, weight, height, postoperative intensive care unit length of stay, total hospital stay, and post-operative complications (Low cardiac output synd. Inotropy-IABP requirement, insulin-dependent diabetes mellitus, arrhythmia, kidney failure, respiratory failure) were recorded. In the histopathological evaluation, the expression density of Nesfatin-1, Galectin-3, Ghrelin, and Leptin in the the adipose tissue samples were mainly examined.Results:There was no statistically significant difference between the expression of Galectin-3, Ghrelin, and Leptin with post-operative complications, length of stay in the intensive care unit, and body mass index in patients with and without metabolic syndrome. However, there is a significant difference between Nesfatin-1 expression and the risk of postoperative complications, length of stay in intensive care unit and metabolic syndrome (respectively p=0.026, p=0.030, p=0.047).Conclusion:Nesfatin-1 plays a role in glucose homeostasis as a negative regulator of glucose levels. In this study, it is thought that patients with low body mass index and high Nefsatin-1 expression may have a better postoperative clinical course.

Introduction:Although nutrition is very effective on mortality in critically ill children, patients cannot be fed adequately. There is no suitable biomarker for enteral nutrition monitoring and management. The aim of this study; To investigate the usability of nefsatin-1 for nutritional monitoring and management in critically ill children.Methods:In the January-September 2019 period, 35 critically ill children who were hospitalized in the tertiary pediatric intensive care unit without any signs of inflammation were included in the study. Nesfatin-1, vitamin D level, prealbumin, albumin was evaluated for the study.Results:Thirty-five patients who were admitted to the pediatric intensive care unit and whose hospitalization reasons had regressed were evaluated. The mean nesfatin-1 values of the patients were measured as 9.95±0.78 ng/mL (4.25-18.93 ng/mL). There was a negative and low (r=-0.214) relationship between target calorie intake and nesfatin-1, a positive and low (r=0.172) relationship with prealbumin, and a positive and high relationship with vitamin D (r=0.529). Similar relationships were determined between the weight change ratio and nesfatin-1 (r=-0.266), prealbumin (r=0.154) and vitamin D (r=0.337).Conclusion:Based on the study findings, it was concluded that serum nefsatin-1, albumin and prealbumin are not appropriate indicators for nutritional monitoring and management in critically ill children.

Sleep contributes to the energy balance of body. This study aims to investigate how rapid eye movement (REM) sleep deprivation (SD) or recovery sleep affects rat weight and the serum levels of Nesfatin-1, Orexin-A, and Leptin; additionally, seeks to determine the impact of melatonin administration on these parameters. Male, Sprague Dawley rats were randomized into two groups (n=9). REMSD was induced using the modified multiple platform method (MMPM). Melatonin was used as a treatment (20 mg/kg). Study Group I was created to investigate the effectiveness of the treatment during REMSD. Study Group II was established to analyze the possible therapeutic role of melatonin and recovery sleep after REMSD-induced damage. The rats' weights were recorded during the experiments. Blood samples were collected from all rats via decapitation after experiments. The levels of serum Nesfatin-1, Orexin-A, and Leptin were analyzed using the ELISA method. REMSD affected weight of the rats and altered the levels of serum Nesfatin-1 and Leptin. Melatonin administration influenced weight gain and affected Nesfatin-1 and Leptin levels. REMSD or melatonin did not affect Orexin-A levels. REMSD and melatonin play significant roles in the body's energy balance. This study will contribute to elucidating the role of SD in metabolic processes and will play a role in assessing the impact of melatonin, a commonly used treatment in human and veterinary medicine. [ABSTRACT FROM AUTHOR]

In this study, we propose a simple, cost-effective, and sensitive high-performance liquid chromatography with both detection techniques such as diode-array detection and fluorescence detection (HPLC-DAD-FLD) for the determination of nesfatin-1 in fetal bovine serum samples. The limit of detection (LOD) and limit of quantification (LOQ) for nesfatin-1 were set at satisfactory values in the range 0.22–0.35 mg mL−1 and in the range 0.67–1.05 mg mL−1, respectively (at two different wavelengths (DAD) and at four different wavelengths (FLD)). Analyte concentrations were determined as the average value from fetal bovine serum matrix samples. The preliminary results show that the SPE procedure on Isolute Si-TsOH (SCX-3) could be used for further nesfatin-1 analyses in human serum samples. Both the SPE technique, chromatographic analysis with gradient elution mode and detection technique are fast and convenient. [ABSTRACT FROM AUTHOR]

Background: Hashimoto's thyroiditis (HT) is an autoimmune disorder affecting the thyroid gland and may present as goiter or atrophic thyroiditis that may result in various metabolic and inflammatory disorders. The aim of this study is to determine the changes in serum levels of inter- leukin-17 (IL-17), IL-23, neopterin, and nesfatin-1 parameters in HT patients and to evaluate the possible relationship among these parameters. Methods: 90 HT patients and 30 healthy individuals were included in this study. Demographic data of the patients included in the study were recorded and detailed physical examinations were performed. IL-17, IL-23, neopterin, and nesfatin-1 levels were measured in the serum samples of the participants by the ELISA method. Results: Serum IL-17, IL-23, neopterin, levels were significantly higher and nesfatin-1 levels were significantly lower in the HT group compared to the control group. Statistically significant differences were observed between all the groups except euthyroid HT versus HT treated with levothyroxine for nesfatin-1 at the 0.05 level. Conclusion: IL-17, IL-23, and neopterin were involved in the etiopathogenesis of HT. Weight gain in HT may due to low nesfatin-1 level rather than throid hormone deficiency. These variables could be used as potential biomarkers in the diagnosis, prognosis and fellow up of HT disease. [ABSTRACT FROM AUTHOR]

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Abstract Autophagy and cytoskeleton integrity of chondrocytes are a considered as major factors in the progression of osteoarthritis (OA) involving excessive chondrocyte apoptosis and senescence. Nesfatin-1, an adipokine, has been reported to be closely related to cell autophagy and cytoskeleton malfunction. Our previous study found that nesfatin-1 was highly correlated with OA progress in OA patient, and the expression of nesfatin-1 rises in knee articular tissue, serum and chondrocytes. In current study, we aimed to explore the therapeutic effect of nesfatin-1 on OA and its molecular mechanism related to chondrocyte autophagy and cytoskeleton malfunction. We firstly demonstrated that nesfatin-1 effectively suppressed excessive autophagy of OA chondrocytes at both gene and protein levels. Meanwhile, we also found that nesfatin-1 significantly improved cytoskeleton integrity by showing higher F-actin/G-actin ratio, as well as more organized actin fiber structure. Mechanistically, utility of RhoA activator and inhibitor revealed that regulation of autophagy and cytoskeleton integrity via nesfatin-1 was realized via RhoA/ROCK pathway. We also confirmed that nesfatin-1 significantly ameliorated IL-1β induced cartilage degeneration via destabilization of the medial meniscus (DMM) model. Overall, our study indicates that nesfatin-1 might be a promising therapeutic molecule for OA intervention.

Aggression is a prevalent and concerning behavioral issue in dogs. Pit Bull dogs, known for their high levels of aggression, are recognized as a focus of concern in society. In our study, we aimed to investigate the behavioral characteristics of Pit Bull dogs and explore the potential roles of peptides involved in the neurobiology of aggression. Initially, female, and male dogs underwent aggression tests, and their aggression levels were categorized. Plasma nesfatin-1, serotonin, oxytocin, and dopamine levels were quantified using ELISA, with blood samples collected after a 24 h fasting period and 2 h post-refeeding. Our findings indicate that aggression in Pit Bull dogs correlates with decreased plasma nesfatin-1, serotonin, and oxytocin levels, while dopamine levels increase. The study’s findings indicate that fasted dogs exhibited lower plasma levels of nesfatin-1, serotonin, and dopamine, while plasma oxytocin levels were higher. Furthermore, while the research findings do not suggest a significant relationship between the severity of aggression and the gender of the dog, male Pit Bull breeds appear to have higher plasma nesfatin-1 and serotonin levels compared to their female counterparts. The study’s findings demonstrate that nesfatin-1, serotonin, oxytocin, and dopamine play pivotal roles in Pit Bull dogs’ aggression, indicating potential interactions among these neuropeptides at the central nervous system level.