Nesfatin-1 increases intracellular calcium concentration by protein kinase C activation in cultured rat dorsal root ganglion neurons

Ozcan, Mete; Gök, Zeynep Betül; Kacar, Emine; Serhatlioğlu, İhsan; Keleştimur, Haluk

doi:10.1016/j.neulet.2016.03.018

Cited by 17 publications

(11 citation statements)

References 24 publications

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“…For the first time, nesfatin-1 and its related encoding gene and precursors were identified by Oh and his group in 2006 (1). This neuropeptide is the result of encoding of the N-terminal region of protein precursor, Nucleobindin2 (NUCB2), and the major sites of its expression are the hypothalamus and other areas of the brain, gastric endocrine cells, pancreatic islets, and adipocytes (2)(3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Serum Nesfatin-1 Level in Healthy Subjects with Weight-Related Abnormalities and Newly Diagnosed Patients with Type 2 Diabetes Mellitus; a Case-Control Study

et al. 2019

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Context. Nesfatin-1 is a novel peptide with both central and peripheral anorexigenic regulatory properties. Besides its effects on food intake, few studies have suggested a possible role for this peptide in the pathogenesis of diabetes mellitus type 2. Objective. To compare serum levels of nesfatin-1 between healthy, normal-weight persons and three groups including healthy underweight, healthy obese and diabetic subjects. Design. Prospective, case-control study, performed between January 2015 and January 2016. Subjects and Methods. Fasting levels in serum nesfatin-1 were measured in 30 healthy, normal-weight individuals (controls), 30 healthy underweight persons, 30 healthy obese persons, and 30 patients with newly diagnosed diabetes type 2 using standard enzyme-linked immunosorbent assay (ELISA) kits. Results. The mean serum nesfatin-1 level was significantly higher in controls (2.61 ng/mL) compared to that in obese (1.13 ng/mL) and diabetic (0.99 ng/mL) patients; and significantly lower than that in the underweight group (3.50 ng/mL). The obese and diabetic groups were comparable in this regard. No significant association was found between serum nesfatin-1 level and age, sex, or body mass index. Conclusions. Serum nesfatin-1 is possibly associated with weight-related abnormalities in otherwise healthy subjects and diabetes type 2. Obesity and diabetes type 2 may share a common pathologic point in this regard.

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Section: Introductionmentioning

confidence: 99%

Serum Nesfatin-1 Level in Healthy Subjects with Weight-Related Abnormalities and Newly Diagnosed Patients with Type 2 Diabetes Mellitus; a Case-Control Study

et al. 2019

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“…Another calcium binding protein with a highly differentiated SNP (rs757081) was NUCB2. NUCB2 shares a 60% sequence homology with NUCB1 in the human and mouse genome [41] and plays an important role in homeostatic functions associated with stress response [42], where its expression increased intracellular calcium concentration by protein kinase C activation in cultured rat cultured rat dorsal root ganglion neurons [43]. This SNP has also been associated with systolic blood pressure, mean arterial pressure and pulse pressure in individuals with European ancestry [44], and in African Americans it has been associated with both Feature key refer to the Post-translational modifications (PTM) events in the protein and position refer to the PTM events position in the protein systolic and diastolic blood pressure [45].…”

Section: Discussionmentioning

confidence: 99%

Selected neuropeptide genes show genetic differentiation between Africans and non-Africans

et al. 2020

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Background: Publicly available genome data provides valuable information on the genetic variation patterns across different modern human populations. Neuropeptide genes are crucial to the nervous, immune, endocrine system, and physiological homeostasis as they play an essential role in communicating information in neuronal functions. It remains unclear how evolutionary forces, such as natural selection and random genetic drift, have affected neuropeptide genes among human populations. To date, there are over 100 known human neuropeptides from the over 1000 predicted peptides encoded in the genome. The purpose of this study is to analyze and explore the genetic variation in continental human populations across all known neuropeptide genes by examining highly differentiated SNPs between African and non-African populations. Results: We identified a total of 644,225 SNPs in 131 neuropeptide genes in 6 worldwide population groups from a public database. Of these, 5163 SNPs that had ΔDAF |(African-non-African)| ≥ 0.20 were identified and fully annotated. A total of 20 outlier SNPs that included 19 missense SNPs with a moderate impact and one stop lost SNP with high impact, were identified in 16 neuropeptide genes. Our results indicate that an overall strong population differentiation was observed in the non-African populations that had a higher derived allele frequency for 15/20 of those SNPs. Highly differentiated SNPs in four genes were particularly striking: NPPA (rs5065) with high impact stop lost variant; CHGB (rs6085324, rs236150, rs236152, rs742710 and rs742711) with multiple moderate impact missense variants; IGF2 (rs10770125) and INS (rs3842753) with moderate impact missense variants that are in linkage disequilibrium. Phenotype and disease associations of these differentiated SNPs indicated their association with hypertension and diabetes and highlighted the pleiotropic effects of these neuropeptides and their role in maintaining physiological homeostasis in humans. Conclusions: We compiled a list of 131 human neuropeptide genes from multiple databases and literature survey. We detect significant population differentiation in the derived allele frequencies of variants in several neuropeptide genes in African and non-African populations. The results highlights SNPs in these genes that may also contribute to population disparities in prevalence of diseases such as hypertension and diabetes.

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“…Both neuronal depolarization (Brailoiu et al 2013) as well as the increase in intracellular Ca 2+ (Brailoiu et al 2007, Ozcan et al 2016 were prevented by pretreatment with pertussis toxin, indicating the involvement of a G i -protein-coupled receptor. Accordingly, no increase 232:1 in cyclic adenosine monophosphate (cAMP) formation was observed (Ishida et al 2012).…”

Section: Nesfatin-1: Signal Transductionmentioning

confidence: 94%

“…The activation of protein kinase A (PKA) appears to differ across tissues and might indicate a tissue-specific recruitment of G-protein subunits (Brailoiu et al 2007, Nakata et al 2011, Ishida et al 2012. In addition to these established G-protein-related pathways, in cardiac myocytes and DRG neurons, nesfatin-1 acts to inhibit L-type Ca 2+ channels through protein kinase C (PKC), indicating an involvement of G q (Ying et al 2015, Ozcan et al 2016. These findings, albeit unequivocal with regard to the type of G-proteins involved, suggest the existence of one or more 7-transmembrane receptor(s).…”

Section: Nesfatin-1: Signal Transductionmentioning

confidence: 99%

Nesfatin-1: functions and physiology of a novel regulatory peptide

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

114

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Nesfatin-1 was identified in 2006 as a potent anorexigenic peptide involved in the regulation of homeostatic feeding. It is processed from the precursor-peptide NEFA/ nucleobindin 2 (NUCB2), which is expressed both in the central nervous system as well as in the periphery, from where it can access the brain via non-saturable transmembrane diffusion. In hypothalamus and brainstem, nesfatin-1 recruits the oxytocin, the melancortin and other systems to relay its anorexigenic properties. NUCB2/nesfatin-1 peptide expression in reward-related areas suggests that nesfatin-1 might also be involved in hedonic feeding. Besides its initially discovered anorexigenic properties, over the last years, other important functions of nesfatin-1 have been discovered, many of them related to energy homeostasis, e.g. energy expenditure and glucose homeostasis. Nesfatin-1 is not only affecting these physiological processes but also the alterations of the metabolic state (e.g. fat mass, glycemic state) have an impact on the synthesis and release of NUCB2 and/or nesfatin-1. Furthermore, nesfatin-1 exerts pleiotropic actions at the level of cardiovascular and digestive systems, as well as plays a role in stress response, behavior, sleep and reproduction. Despite the recent advances in nesfatin-1 research, a putative receptor has not been identified and furthermore potentially distinct functions of nesfatin-1 and its precursor NUCB2 have not been dissected yet. To tackle these open questions will be the major objectives of future research to broaden our knowledge on NUCB2/nesfatin-1.

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Nesfatin-1 increases intracellular calcium concentration by protein kinase C activation in cultured rat dorsal root ganglion neurons

Cited by 17 publications

References 24 publications

Serum Nesfatin-1 Level in Healthy Subjects with Weight-Related Abnormalities and Newly Diagnosed Patients with Type 2 Diabetes Mellitus; a Case-Control Study

Serum Nesfatin-1 Level in Healthy Subjects with Weight-Related Abnormalities and Newly Diagnosed Patients with Type 2 Diabetes Mellitus; a Case-Control Study

Selected neuropeptide genes show genetic differentiation between Africans and non-Africans

Nesfatin-1: functions and physiology of a novel regulatory peptide

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