Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Xia, Ze Feng; Fritze, Danielle; Li, Ji Yao; Chai, Biaoxin; Zhang, Chao; Zhang, Weizhen; Mulholland, Michael W.

doi:10.1152/ajpgi.00178.2012

Cited by 46 publications

(31 citation statements)

References 50 publications

(51 reference statements)

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“…Particularly, a central injection of an anorexigenic dose of nesfatin-1 is also capable to inhibit the 2-deoxy-d-glucose-stimulated gastric acid secretion via vagal efferents in rats, as suggested by a 16-fold increase of c-fos-positive neurons in the DMNX, but not in the NTS (Xia et al 2012). In agreement, 80% of DMNX neurons projecting to the stomach are nesfatin-1 positive (as was shown by retrograde tracing) (Bonnet et al 2013).…”

Section: Gastric Distension and Gastric Acid Secretionsupporting

confidence: 71%

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

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

117

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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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Section: Gastric Distension and Gastric Acid Secretionsupporting

confidence: 71%

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

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

117

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show abstract

“…Gastric NUCB2/ nesfatin-1 mRNA expression levels were higher than expression levels in other peripheral organs and brain (48). Nesfatin-1 reduced the release of gastric acid in a dose-dependent manner and influenced gastrointestinal motility (2,24,55,58). Its presence in pancreatic cells was detected particularly in the beta cells of Langerhans islets (15,27).…”

Section: Artykuł Przeglądowy Reviewmentioning

confidence: 97%

Role of nesfatin-1 in the metabolism of skeletal tissues

Puzio¹,

Tymicki²,

Predka³

et al. 2018

Medycyna Weterynaryjna

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Puzio I., Tymicki G., Predka H., Śleboda W., Sobczyńska-Wołejszo M.Role of nesfatin-1 in the metabolism of skeletal tissues Summary NUCB2/nesfatin-1, a member of the adipokine family, is a peptide hormone with pleiotropic action. It has been found in different tissues, including cartilage and bone cells. Nesfatin-1 is produced by chondrocytes, and its synthesis increases with the degree of cell differentiation and upon stimulation by pro-inflammatory cytokines, as shown in an in vitro study. An increase in serum levels of nesfatin-1 has been observed in humans with osteoarthritis, which indicates the influence of pro-inflammatory cytokines on nesfatin-1 release. On the other hand, nesfatin-1 stimulates the synthesis of pro-inflammatory cytokines by chondrocytes, which suggests its participation, together with other adipokines, in the pathogenesis and/or progression of inflammatory complications of cartilage degenerative diseases. Nesfatin-1 also promotes pre-osteoblastic cell differentiation and mineralization and inhibits macrophage differentiation towards osteoclasts. Moreover, exogenous nesfatin-1 given to ovariectomized rats reduces osteopenic changes. Therefore, it seems that nesfatin-1 may play a protective role in cartilage and bone diseases. However, further studies are required to determine whether nesfatin-1 can be used for monitoring and treatment of cartilage and bone diseases.

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“…Existing evidence using Ca 2+ flux as an index suggested that NUCB2/nesfatin-1’s action in neurons is mediated by a Gi/o-protein-coupled receptor as the response is abolished by pertussis toxin [7, 14]. In particular, in vitro studies showed that nesfatin-1 stimulates Ca 2+ influx into neurons of the rat hypothalamus [7, 15], rat dorsal motor nucleus of the vagus nerve (DMV) [16], and mouse vagal afferent nodose ganglion [17]. Results obtained using inhibitors specific for subtypes of Ca 2+ channels indicate that the nesfatin-1-induced elevation of [Ca 2+ ] i exhibits pharmacological characteristics of either N-, L-, and/or P/Q channels.…”

Section: Introductionmentioning

confidence: 99%

Role of NUCB2/Nesfatin-1 in the Hypothalamic Control of Energy Homeostasis

Stengel

Taché

2013

Horm Metab Res

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Hunger and satiety are regulated in a complex fashion by a few food intake stimulatory (orexigenic) and a multitude of inhibitory (anorexigenic) factors produced in the periphery (mainly in the gastrointestinal tract) or directly in the brain. Within the brain, the hypothalamus plays a pivotal role as a production site of food intake regulatory factors. Importantly, this site integrates peripheral and central signaling factors to orchestrate food intake and in the long term body weight. Our knowledge on these regulatory pathways is not static but rather rapidly changing as new factors as well as upand downstream signaling pathways of already known transmitters are uncovered. Hypothalamic nucleobindin2 (NUCB2), the precursor of nesfatin-1, was first described in 2006 and nesfatin-1 found to be a novel anorexigenic modulator of food intake and body weight. The initial report stimulated several groups to investigate the biological actions of nesfatin-1 and subsequent studies delineated the underlying brain mechanisms involved in its food reducing effect. Of interest was the demonstration that NUCB2 also exerts its anorexigenic action in the paraventricular nucleus of the hypothalamus and is regulated at this site by changes in metabolic status with a diurnal rhythm inversely related to that of feeding in rats. The present review describes the current state-of-knowledge on central nesfatin-1’s effects on food intake and body weight and highlights important missing links regarding cellular signaling mechanisms involved in nesfatin-1’s action.

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Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Cited by 46 publications

References 50 publications

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

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

Role of nesfatin-1 in the metabolism of skeletal tissues

Role of NUCB2/Nesfatin-1 in the Hypothalamic Control of Energy Homeostasis

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