The Physiological Relationships Between the Brainstem, Vagal Stimulation, and Feeding

Stengel, Andreas; Taché, Yvette

doi:10.1007/978-0-387-92271-3_54

Cited by 7 publications

(6 citation statements)

References 79 publications

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“…These data, along with mapping of medullary Fos positive neurons in response to intraperitoneal injection of nesfatin-1, support the assumption that peripheral nesfatin-1 can influence the activity of vagal afferents and possibly suppress feeding by activating POMC and CART neurons in the NTS [31]. Therefore, data so far support a peripheral nesfatin-1 signaling pathway that may involve the vagus nerve consistent with the prominent expression of NUCB2/nesfatin-1 in the stomach and the vagal mediation commonly established for other gut satiety peptides [33]. …”

Section: Inhibition Of Food Intake Body Weight and Digestive Funcsupporting

confidence: 67%

Nesfatin-1 — Role as possible new potent regulator of food intake

Stengel

Taché

2010

Regulatory Peptides

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Nesfatin-1 is an 82 amino acid peptide recently discovered in the brain which is derived from nucleobindin2 (NUCB2), a protein that is highly conserved across mammalian species. Nesfatin-1 has received much attention over the past two years due to its reproducible food intake-reducing effect that is linked with recruitment of other hypothalamic peptides regulating feeding behavior. A growing amount of evidence also supports that various stressors activate fore- and hindbrain NUCB2/nesfatin-1 circuitries. In this review, we outline the central nervous system distribution of NUCB2/nesfatin-1, and recent developments on the peripheral expression of NUCB2/nesfatin-1, in particular its co-localization with ghrelin in gastric X/A-like cells and insulin in β-cells of the endocrine pancreas. Functional studies related to the characteristics of nesfatin-1’s inhibitory effects on dark phase food intake are detailed as well as the central activation of NUCB2/nesfatin-1 immunopositive neurons in the response to psychological, immune and visceral stressors. Lastly, potential clinical implications of targeting NUCB2/nesfatin-1 signaling and existing gaps in knowledge to ascertain the role and mechanisms of action of nesfatin-1 are presented.

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Section: Inhibition Of Food Intake Body Weight and Digestive Funcsupporting

confidence: 67%

Nesfatin-1 — Role as possible new potent regulator of food intake

Stengel

Taché

2010

Regulatory Peptides

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“…This activation is likely associated with the increased interaction with food (as reflected in the increased number of bouts in activity-based anorexia rats compared to the ad libitum group) as well as the stimulated food intake during the 1.5-h feeding period. In line with this assumption, key areas of food intake regulation were activated as well, namely the lateral septal nucleus (Mitra et al, 2015), lateral hypothalamic area (Bernardis and Bellinger, 1993), the dorsomedial hypothalamic nucleus and the medial part of the Arc, both expressing the potent orexigenic transmitter neuropeptide Y (Wang et al, 2002; Bi et al, 2012) and lastly also the nucleus of the solitary tract (Stengel and Taché, 2011). Further corroborating the involvement of these nuclei in the orexigenic drive under conditions of activity-based anorexia, a previous study reported a robust upregulation of orexigenic agouti-related peptide and neuropeptide Y, whereas the anorexigenic transmitters pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) were reduced in the Arc of activity-based anorexia rats compared to sedentary food-restricted controls (de Rijke et al, 2005).…”

Section: Discussionmentioning

confidence: 83%

“…Moreover, in the lateral hypothalamic area melanin-concentrating hormone mRNA expression was increased in activity-based anorexia rats (de Rijke et al, 2005). Associated with the orexigenic response, also brain nuclei involved in the regulation of gastrointestinal motility were activated, namely the lateral hypothalamic area (Gong et al, 2013), nucleus of the solitary tract and the dorsal motor nucleus of the vagus nerve (Stengel and Taché, 2011). This pronounced activation likely underlies the robust orexigenic response of activity-based anorexia rats observed during the 1.5-h feeding period.…”

Section: Discussionmentioning

confidence: 99%

Activity-Based Anorexia Reduces Body Weight without Inducing a Separate Food Intake Microstructure or Activity Phenotype in Female Rats—Mediation via an Activation of Distinct Brain Nuclei

et al. 2016

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Anorexia nervosa (AN) is accompanied by severe somatic and psychosocial complications. However, the underlying pathogenesis is poorly understood, treatment is challenging and often hampered by high relapse. Therefore, more basic research is needed to better understand the disease. Since hyperactivity often plays a role in AN, we characterized an animal model to mimic AN using restricted feeding and hyperactivity. Female Sprague-Dawley rats were divided into four groups: no activity/ad libitum feeding (ad libitum, AL, n = 9), activity/ad libitum feeding (activity, AC, n = 9), no activity/restricted feeding (RF, n = 12) and activity/restricted feeding (activity-based anorexia, ABA, n = 11). During the first week all rats were fed ad libitum, ABA and AC had access to a running wheel for 24 h/day. From week two ABA and RF only had access to food from 9:00 to 10:30 a.m. Body weight was assessed daily, activity and food intake monitored electronically, brain activation assessed using Fos immunohistochemistry at the end of the experiment. While during the first week no body weight differences were observed (p > 0.05), after food restriction RF rats showed a body weight decrease: −13% vs. day eight (p < 0.001) and vs. AC (−22%, p < 0.001) and AL (−26%, p < 0.001) that gained body weight (+10% and +13%, respectively; p < 0.001). ABA showed an additional body weight loss (−9%) compared to RF (p < 0.001) reaching a body weight loss of −22% during the 2-week restricted feeding period (p < 0.001). Food intake was greatly reduced in RF (−38%) and ABA (−41%) compared to AL (p < 0.001). Interestingly, no difference in 1.5-h food intake microstructure was observed between RF and ABA (p > 0.05). Similarly, the daily physical activity was not different between AC and ABA (p > 0.05). The investigation of Fos expression in the brain showed neuronal activation in several brain nuclei such as the supraoptic nucleus, arcuate nucleus, locus coeruleus and nucleus of the solitary tract of ABA compared to AL rats. In conclusion, ABA combining physical activity and restricted feeding likely represents a suited animal model for AN to study pathophysiological alterations and pharmacological treatment options. Nonetheless, cautious interpretation of the data is necessary since rats do not voluntarily reduce their body weight as observed in human AN.

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“…Since the vagus nerve is a major driving source of gastrointestinal motility [79], the modulation of vagal activity is an interesting target in order to influence symptoms of abdominal surgery-induced postoperative ileus. It is well known that a reduction in ambient temperature activates the thyrotropin-releasing hormone (TRH) signaling system [80] expressed in the raphe pallidus, raphe obscurus and parapyramidal regions projecting to the dorsal vagal complex of the brainstem [81] resulting in a vagal dependent cholinergic stimulation of gastric motility and secretion through activation of gastric myenteric cholinergic neurons [80].…”

Section: Modulation Of Postoperative Ileus By Brain Peptides and Neurmentioning

confidence: 99%

Brain peptides and the modulation of postoperative gastric ileus

Stengel¹,

Taché²

2014

Current Opinion in Pharmacology

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Postoperative ileus (POI) develops after abdominal surgery irrespective of the site of surgery. When prolonged, POI can lead to longer hospitalization times and higher healthcare costs. Moreover, it is associated with complaints for the patient. In order to develop new strategies to treat this condition, a deeper understanding of the pathophysiology of the POI is necessary. This review will focus on brain peptides (ghrelin, nesfatin-1, somatostatin, corticotropin-releasing factor, thyrotropin-releasing hormone and calcitonin gene-related peptide) involved in the mediation of POI and the possible modulation of these pathways to shorten the time of POI. Lastly, the role of vagal signaling and the possibility of reducing ambient temperature or chewing gum as potential treatment strategies of alleviating symptoms of POI is discussed.

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The Physiological Relationships Between the Brainstem, Vagal Stimulation, and Feeding

Cited by 7 publications

References 79 publications

Nesfatin-1 — Role as possible new potent regulator of food intake

Nesfatin-1 — Role as possible new potent regulator of food intake

Activity-Based Anorexia Reduces Body Weight without Inducing a Separate Food Intake Microstructure or Activity Phenotype in Female Rats—Mediation via an Activation of Distinct Brain Nuclei

Brain peptides and the modulation of postoperative gastric ileus

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