Ghrelin augments afferent response to distension in rat isolated jejunum

Murray, Charles; Booth, Charlotte E.; Bulmer, D; Kamm, Michael A.; Emmanuel, Anton; Winchester, Wendy J.

doi:10.1111/j.1365-2982.2006.00848.x

Cited by 10 publications

(5 citation statements)

References 20 publications

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“…A reduced acyl ghrelin level has been correlated with impaired gastric emptying (Shindo et al, 2009 ) which can lead to postprandial fullness and vomiting (Stanghellini et al, 1996 ); diagnostic symptoms for functional dyspepsia. Growth hormone secretagogue receptor type 1a, the receptor for ghrelin, is expressed in the nodose ganglia (Burdyga et al, 2006 ) and ghrelin has been shown to increase and decrease responses to distension in the jejunum (Murray et al, 2006 ) and stomach (Page et al, 2007 ) respectively. This suggests specific vagal afferent populations respond differently to ghrelin.…”

Section: Functional Dyspepsia and Vagal Afferent Signalingmentioning

confidence: 99%

Meal-Sensing Signaling Pathways in Functional Dyspepsia

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2018

Front. Syst. Neurosci.

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The upper gastrointestinal tract plays an important role in sensing the arrival, amount and chemical composition of a meal. Ingestion of a meal triggers a number of sensory signals in the gastrointestinal tract. These include the response to mechanical stimulation (e.g., gastric distension), from the presence of food in the gut, and the interaction of various dietary nutrients with specific “taste” receptors on specialized enteroendocrine cells in the small intestine culminating in the release of gut hormones. These signals are then transmitted to the brain where they contribute to food intake regulation by modulating appetite as well as feedback control of gastrointestinal functions (e.g., gut motility). There is evidence that the sensitivity to these food related stimuli is abnormally enhanced in functional dyspepsia leading to symptoms such nausea and bloating. In addition, these gut-brain signals can modulate the signaling pathways involved in visceral pain. This review will discuss the role of gut-brain signals in appetite regulation and the role dysregulation of this system play in functional dyspepsia.

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Section: Functional Dyspepsia and Vagal Afferent Signalingmentioning

confidence: 99%

Meal-Sensing Signaling Pathways in Functional Dyspepsia

Page

2018

Front. Syst. Neurosci.

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“…Functional ablation of VAN via perineural capsaicin treatment, total subdiaphragmatic or selective gastric vagotomy inhibits the ability of ghrelin to increase food intake in mice and rats (5, 8–9) and truncal vagotomy associated with gastric surgery inhibited the stimulatory effect of ghrelin in humans (10), although this has been not been verified in one study in rats (11). In addition, ghrelin has been shown to influence VAN function; ghrelin inhibits the neuronal discharge of gastric mechanoreceptor fibers and increases the discharge of subdiaphragmatic vagal afferents innervating the intestine to distention stimulus (12–13). …”

Section: 0 Introductionmentioning

confidence: 99%

Effect of ghrelin receptor antagonist on meal patterns in cholecystokinin type 1 receptor null mice

Lee

Martin

Paulino

et al. 2011

Physiology & Behavior

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Vagal afferent neurons (VAN) express the cholecystokinin (CCK) type 1 receptor (CCK1R) and, as predicted by the role of CCK in inducing satiation, CCK1R−/− mice ingest larger and longer meals. However, after a short fast, CCK1R−/− mice ingesting high fat (HF) diets initiate feeding earlier than wild-type mice. We hypothesized that the increased drive to eat in CCK1R−/− mice eating HF diet is mediated by ghrelin, a gut peptide that stimulates food intake. The decrease in time to first meal, and the increase in meal size and duration in CCK1R−/− compared to wild-type mice ingesting high fat (HF) diet was reversed by administration of GHSR1a antagonist D-(Lys3)-GHRP-6 (p<0.05). Administration of the GHSR1a antagonist significantly increased expression of the neuropeptide cocaine and amphetamine-regulated transcript (CART) in VAN of HF-fed CCK1R−/− but not wild-type mice. Administration of the GHSR1a antagonist decreased neuronal activity measured by immunoreactivity for fos protein in the nucleus of the solitary tract (NTS) and the arcuate nucleus of both HF-fed wild-type and CCK1R−/− mice. The data show that hyperphagia in CCK1R−/− mice ingesting HF diet is reversed by blockade of the ghrelin receptor, suggesting that in the absence of the CCK1R, there is an increased ghrelin-dependent drive to feed. The site of action of ghrelin receptors is unclear, but may involve an increase in expression of CART peptide in VAN in HF-fed CCK1R−/− mice.

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“…CCK is involved in a variety of physiological functions, some of which overlap with those of the MCH system. CCK is anxiogenic (de Montigny, ; Murray et al, ), and icv MCH injections promote anxiety‐like behavior (Smith et al, ). Paradoxically, CCK has also been reported to suppress feeding (Schick et al, ), whereas MCH is orexigenic, so how the two systems might interact to regulate feeding behavior is unclear.…”

Section: Discussionmentioning

confidence: 99%

Identification of neuropeptide receptors expressed by melanin‐concentrating hormone neurons

Parks

Wang

et al. 2014

J of Comparative Neurology

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Melanin-concentrating Hormone (MCH) is a 19 amino acid cyclic neuropeptide that acts in rodents via the MCH receptor 1 (MCHR1) to regulate a wide variety of physiological functions. MCH is produced by a distinct population of neurons located in the lateral hypothalamus (LH) and zona incerta (ZI) but MCHR1 mRNA is widely expressed throughout the brain. The physiological responses and behaviors regulated by the MCH system have been investigated, but less is known about how MCH neurons are regulated. The effects of most classical neurotransmitters on MCH neurons have been studied, but those of neuropeptides are poorly understood. In order to gain insight into how neuropeptides regulate the MCH system, we investigated which neuropeptide receptors are expressed by MCH neurons using double in situ hybridization. In all, twenty receptors, selected based upon either a suspected interaction with the MCH system or demonstrated high expression levels in the LH and ZI, were tested to determine whether they are expressed by MCH neurons. Overall, eleven neuropeptide receptors were found to exhibit significant colocalization with MCH neurons: Nociceptin / Orphanin FQ Opioid receptor (NOP), MCHR1, both Orexin receptors (ORX), Somatostatin receptor 1 and 2 (SSTR1, SSTR2), the Kisspeptin receotor (KissR1), Neurotensin receptor 1 (NTSR1), Neuropeptide S receptor (NPSR), Cholecystokinin receptor A (CCKAR) and the κ-opioid receptor (KOR). Of these receptors, six have never before been linked to the MCH system. Surprisingly, several receptors thought to regulate MCH neurons displayed minimal colocalization with MCH, suggesting that they may not directly regulate the MCH system.

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Ghrelin augments afferent response to distension in rat isolated jejunum

Cited by 10 publications

References 20 publications

Meal-Sensing Signaling Pathways in Functional Dyspepsia

Meal-Sensing Signaling Pathways in Functional Dyspepsia

Effect of ghrelin receptor antagonist on meal patterns in cholecystokinin type 1 receptor null mice

Identification of neuropeptide receptors expressed by melanin‐concentrating hormone neurons

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