Neuropeptide W: An Anorectic Peptide Regulated by Leptin and Metabolic State

Date, Yukari; Mondal, Muhtashan S.; Kageyama, Haruaki; Ghamari‐Langroudi, Masoud; Takenoya, Fumiko; Yamaguchi, Hideki; Shimomura, Yukio; Mori, Masataka; Murakami, Noboru; Sato, Seiji; Cone, Roger D.; Nakazato, Masamitsu

doi:10.1210/jcem.95.3.9990

Cited by 7 publications

(19 citation statements)

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“…It has been reported that rat NPW mRNA is expressed in the hypothalamus, pituitary gland and adrenal gland [6]. NPW is thought to play a role in the regulation of feeding behavior, energy homeostasis [2,[7][8][9], neuroendocrine regulation [2,3,10], autonomic regulation [11] and inflammatory pain [12,13]. In terms of its neuroendocrine roles, it has been reported that icv administration of NPW elevates plasma PRL and corticosterone levels and lowers GH levels [3].…”

Section: Discussionmentioning

confidence: 99%

“…ACTH release from the anterior pituitary is regulated by hypothalamic factors such as CRF and AVP [14]. NPBWR1 mRNA was reported to be expressed in the paraventricular nucleus (PVN) [15][16][17], and both an NPW transcript and NPW-immunoreactive neurons were observed in the parvocellular division of PVN where CRF and AVP neurons coexist [7]. They suggest that activation of the HPA axis by NPW may occur via CRF or AVP.…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide W stimulates adrenocorticotrophic hormone release via corticotrophin-releasing factor but not via arginine vasopressin

et al. 2012

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Neuropeptide W (NPW) was isolated as an endogenous ligand for NPBWR1, an orphan G protein-coupled receptor localized in the rat brain, including the paraventricular nucleus. It has been reported that central administration of NPW stimulates corticosterone secretion in rats. We hypothesized that NPW activates the hypothalamic-pituitary-adrenal (HPA) axis via corticotrophin-releasing factor (CRF) and/or arginine vasopressin (AVP). NPW at 1 pM to 10 nM did not affect basal or ACTH-induced corticosterone release from dispersed rat adrenocortical cells, or basal and CRF-induced ACTH release from dispersed rat anterior pituitary cells. In conscious and unrestrained male rats, intravenous administration of 2.5 and 25 nmol NPW did not affect plasma ACTH levels. However, intracerebroventricular (icv) administration of 2.5 and 5.0 nmol NPW increased plasma ACTH levels in a dose-dependent manner at 15 min after stimulation (5.0 vs. 2.5 nmol NPW vs. vehicle: 1802 ± 349 vs. 1170 ± 204 vs. 151 ± 28 pg/mL, respectively, mean ± SEM). Pretreatment with astressin, a CRF receptor antagonist, inhibited the increase in plasma ACTH levels induced by icv administration of 2.5 nmol NPW at 15 min (453 ± 176 vs. 1532 ± 343 pg/mL, p<0.05) and at 30 min (564 ± 147 vs. 1214 ± 139 pg/mL, p<0.05) versus pretreatment with vehicle alone. However, pretreatment with [1-(β-mercapto-β, β-cyclopentamethylenepropionic acid), 2-(Ο-methyl)tyrosine]-arg-vasopressin, a V1a/V1b receptor antagonist, did not affect icv NPW-induced ACTH release at any time (p>0.05). In conclusion, we suggest that central NPW activates the HPA axis by activating hypothalamic CRF but not AVP.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neuropeptide W stimulates adrenocorticotrophic hormone release via corticotrophin-releasing factor but not via arginine vasopressin

et al. 2012

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“…Two endogenous molecular isoforms of NPW ligands that consist of 23-and 30-amino acid residues and bind with similar affinity to their receptors were reported [7,8]. The NPW and their receptors are highly expressed in several discrete regions of the rodent brain, including the hypothalamic paraventricular nucleus (PVN), arcuate nucleus (ARC), ventromedial nucleus (VMH) and lateral hypothalamus (LH) [9,10]. The fact that brain administered NPW caused a dose-dependent increase in corticosterone (CORT) levels in rats indicates that NPW may play an important role in the hypothalamic organization of the endocrine response to stress and the modulation of the HPA axis [11].…”

Section: Ivyspringmentioning

confidence: 99%

“…Hypothalamic neurons were processed for immunohistochemically staining as previously described [10]. Rats were first perfused transcardially with 0.1 M phosphate buffer (pH 7.4), then with 4% paraformaldehyde in 0.1 M phosphate buffer.…”

Section: Immunohistochemistry and Immunofluorescencementioning

confidence: 99%

FoxO3a suppresses neuropeptide W expression in neuronal cells and in rat hypothalamus and its implication in hypothalamic-pituitary-adrenal (HPA) axis

Yan¹,

Wang²,

Li³

et al. 2020

Int. J. Biol. Sci.

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FoxO3a, a forkhead family member of transcription factors, is involved in the regulation of cell metabolism, proliferation, differentiation and apoptosis. However, whether FoxO3a participates in the regulation of glucocorticoids induced-hypothalamic-pituitary-adrenal (HPA) dysfunction is still unknown. Our present results indicate that dexamethasone(DEX) increased FoxO3a expression in PC12 and hypothalamic neuronal cultures in correlation to reduced expression of NPW, a process that could be blocked by GR2 antagonist. DEX restrained the phosphorylation of Akt and FoxO3a, but not ERK1/2 phosphorylation, resulting with FoxO3a nuclear localization. Overexpression of FoxO3a inhibited NPW expression, while FoxO3a knockdown by siRNA had the opposite effect. The regulatory region of NPW promoter contains multiple FoxO3a binding sites, and FoxO3a bonding to these sites inhibited its transcriptional activity. In a rat model, chronic administration of corticosterone reduced animals' body weight and sucrose consumption and caused stress-depression like behavior. Corticosterone treatment induced a marked increase in FoxO3a levels, while decreased the expression of NPW protein in the hypothalamus. Immunofluorescent double labeling demonstrated that FoxO3a and NPW were collocated in the hypothalamus. Taken together, these data indicate that NPW is a new direct downstream target gene of FoxO3a. FoxO3a suppressed the transcription of NPW and modulated glucocorticoids-induced HPA dysfunction by directly regulating the expression of NPW. Thus, present findings suggest that FoxO3a and NPW may be potential therapeutic targets for endocrine and psychiatric disorders.

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“…Changes to the synaptic activity of projections from the VMH to proopiomelanocortin (POMC)‐containing neurons in the ARC are known to inhibit feeding behavior 23, 24 and to regulate glucose levels and energy homeostasis 25 . Very recently, Date et al 26 . demonstrated that leptin treatment promotes phosphorylation of STAT3, then induces SOCS‐3 in the NPW‐containing neurons isolated from the VMH.…”

Section: Regulation Of Feeding and Energy Metabolism By Npwmentioning

confidence: 99%

Neuropeptide W: a key player in the homeostatic regulation of feeding and energy metabolism?

Takenoya

Kageyama

Shiba

et al. 2010

Annals of the New York Academy of Sciences

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Neuropeptide W (NPW), recently isolated from porcine hypothalamus, has been identified as the endogenous ligand for both NPBWR1 (GPR7) and NPBWR2 (GPR8), which belong to the orphan G protein-coupled receptor family. NPW is thought to play an important role in the regulation of feeding and drinking behavior, and to be related to the stress response. NPW-containing neurons are localized in several regions of the brain, including the hypothalamus, hippocampus, limbic system, midbrain, and brain stem. Accumulated evidence suggests that hypothalamic neuropeptides, such as neuropeptide Y (NPY), orexin, melanin-concentrating hormone (MCH), and proopiomelanocortin (POMC), are involved in the regulation of feeding behavior and energy homeostasis via neuronal circuits in the hypothalamus. NPW also forms part of the feeding-regulating neuronal circuitry in conjunction with other feeding-regulating peptide-containing neurons within the hypothalamus. We summarize our current understanding of the distribution of NPW and of the neuronal interactions between NPW and the different feeding-regulating peptide-containing neurons. This review also discusses evidence for the dichotomous actions of NPW on energy balance and the potential mechanisms involved.

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Neuropeptide W: An Anorectic Peptide Regulated by Leptin and Metabolic State

Cited by 7 publications

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Neuropeptide W stimulates adrenocorticotrophic hormone release <i>via</i> corticotrophin-releasing factor but not <i>via</i> arginine vasopressin

Neuropeptide W stimulates adrenocorticotrophic hormone release <i>via</i> corticotrophin-releasing factor but not <i>via</i> arginine vasopressin

FoxO3a suppresses neuropeptide W expression in neuronal cells and in rat hypothalamus and its implication in hypothalamic-pituitary-adrenal (HPA) axis

Neuropeptide W: a key player in the homeostatic regulation of feeding and energy metabolism?

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