Ghrelin immunoreactivity in human plasma is suppressed by somatostatin

Nørrelund, Helene; Hansen, Troels Krarup; Ørskov, Hans; Hosoda, Hiroshi; Kojima, Masayasu; Kangawa, Kenji; Weeke, Jørgen; Møller, Niels; Christiansen, Jens Sandahl; Jørgensen, Jens Otto Lunde

doi:10.1046/j.1365-2265.2002.01649.x

Cited by 127 publications

(81 citation statements)

References 49 publications

(64 reference statements)

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“…It is well known that SST has an inhibitory effect on GH, insulin and glucagon release, as well as on many other gastroenteropancreatic hormonal secretions and functions (22,23). SST infusion inhibits ghrelin secretion in humans (23,24). At present, the mechanisms underlying the inhibitory effect of SST on ghrelin secretion are unknown but they likely reflect direct activation of SST receptors in the gastric mucosa (22,23).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori has no effect on plasma ghrelin levels

Gökçel

Gümürdülü

Kayaselçuk

et al. 2003

European Journal of Endocrinology

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Objective: Helicobacter pylori is the major etiologic agent for chronic active gastritis, and it also plays a crucial role in gastric and duodenal ulcer disease, as well as in gastric carcinoma. H. pylori infection has been shown to decrease plasma somatostatin (SST) and increase plasma gastrin concentrations. Ghrelin is a recently discovered peptide produced mostly in the stomach of rodents and humans and is secreted into the bloodstream. There is no data in the literature about the relationship between H. pylori and ghrelin. Design: Thirty-nine age-and BMI-matched H. pylori infection positive and negative women, from whom biopsy specimens were taken during gastric endoscopy, were included in the study. Methods: Total ghrelin was measured by enzyme immunoassay (EIA) in Medistek. All samples were measured in duplicate and averaged; results differing by more than 20% were re-assayed. Two biopsy specimens from antrum, corpus and fundus were obtained. Results: Fifteen of the subjects were H. pylori negative and 24 were H. pylori positive. Age, BMI, lipid profile and insulin sensitivity indices of the groups were similar. Plasma ghrelin levels ð375:92^7:10 vs 370:00^4:14 pmol=l; P . 0:05Þ of H. pylori negative and positive groups did not differ significantly. Conclusion: H. pylori has no effect on plasma ghrelin concentration.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori has no effect on plasma ghrelin levels

Gökçel

Gümürdülü

Kayaselçuk

et al. 2003

European Journal of Endocrinology

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“…Ghrelin secretion has been also inhibited by the activation of somatostatin receptors. The administration of pharmacological doses of somatostatin, its natural analogue cortistatin and a synthetic analogue such as octreotide markedly reduce circulating ghrelin levels in humans to an extent even higher than that observed after glucose or insulin administration [40,41]. Ghrelin, in turn, increases circulating somatostatin levels [42], suggesting the existence of a feedback link between these two peptides.…”

Section: Discussionmentioning

confidence: 99%

Estimation of gastric ghrelin-positive cells activity in hyperthyroid rats.

Dadan

Zbucki²,

Sawicki³

et al. 2009

Folia Histochem Cytobiol.

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Abstract:Ghrelin is a peptide of 28 amino acids that transmits appetite related signals from peripheral organs to the brain. The main source of ghrelin is stomach. The regulation of ghrelin secretion is still unknown. The finding that fasting and food intake, respectively increase and decrease the secretion of ghrelin suggests that this hormone may be a bridge connecting somatic growth with energy metabolism and appears to play an important role in the alteration of energy homeostasis and body weight in pathophisiological conditions. The purpose of this study was the evaluation of gastric ghrelin immunoreactivity and ghrelin plasma concentration in male Wistar rats with hyperthyroidism. Experimental model of hyperthyroidism was induced by intraperitoneal injection of levothyroxine at the dose of 80 μg/kg daily over 21 days. At the end of experiment the animals were anaesthetized, blood was taken from abdominal aorta to determinate plasma ghrelin concentration by RIA and then the animals underwent resection of distal part of stomach. Immunohistochemical study were performed using monoclonal specific antybodies against ghrelin. Hyperthyroidism was a reason of increase of gastric mucosal ghrelin -immunoreactivity, accompanied by a significant decreased of ghrelin plasma concentration. Those observations may indicate, that chronic administration of L-thyroxine cause the change of ghrelin plasma concentration in rats, probably via direct influence on gastric X/A-like cells, but this effect is not responsible for hyperphagia associated with hyperthyroidism.

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“…The most remarkable inhibitory input on ghrelin secretion is represented by the activation of somatostatin (SS) receptors as indicated by evidence that native SS, its natural analog cortistatin, and a synthetic analog such as octreotide lower circulating ghrelin levels in humans [215]. Ghrelin secretion in humans is under the stimulatory control of the cholinergic, namely muscarinic receptors, and acetylcholine is the first stimulatory neurotransmitter shown to play a stimulatory role on ghrelin secretion in humans [216].…”

Section: Regulation Of Ghrelin Secretionmentioning

confidence: 99%

Appetite Regulatory Peptides and Insulin Resistance

Orbetzova¹

2012

Insulin Resistance

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In addition to leptin and insulin, receptors for ghrelin are also located on arcuate AgRP/NPY neurons, which are activated by central ghrelin administration. Furthermore, peripheral ghrelin administration activates neurons in the ARC and AgRP and NPY have been demonstrated to be requisite mediators of the hyperphagia induced by systemic ghrelin [11]. So, meal-generated satiety signals from the GI tract do interact with longer-term adiposity signals, such as insulin and leptin in energy balance [8].NPY is one of the most abundant peptides of the hypothalamus and one of the most potent orexigenic factors. The majority of neurons expressing NPY in the hypothalamus are found within the ARC and most co-express AgRP [14]. Synthesis and release of NPY are both regulated by leptin binding to its hypothalamic receptor. NPY links afferents reflecting the nutritional status of the organism from endocrine, gastrointestinal, and central and peripheral nervous systems to effectors of energy intake and expenditure [15]. NPY stimulates appetite inducing hyperphagia, increase of fat depots, decrease of thermogenesis, and suppression of sympathetic activity. NPY is known to be involved in other physiological functions, such as cardiovascular regulation, affective disorder, memory retention, neuroendocrine control. When leptin levels increase after food intake, the latter binds to its receptors in the hypothalamus which leads to discontinuation of NPY secretion [5,16]. The decrease of NPY concentration in obesity probably plays a role of a counterregulatory factor intended to prevent further weight gain. Thus, NPY becomes one of the main regulators of food intake, body weight and energy expenditure.Ghrelin is a fast-acting hormone, seemingly playing a role in meal initiation. Secreted predominantly from the stomach, ghrelin is the natural ligand for the growth hormone secretagogue-receptor (GHS-R) in the pituitary gland, thus fulfilling the criteria of a brain- gut peptide [5,6]. Although the majority of ghrelin is produced peripherally, there are ghrelin immunoreactive neurons within the hypothalamus that have terminals on hypothalamic NPY/AgRP, POMC and corticotropin releasing hormone (CRH) neurons [17], as well as orexin fibres in the LHA [18]. It was found that ghrelin acts to promote appetite in two ways-directly, by depolarizing the orexigenic NPY/AgRP neurons, and indirectly, by increasing the tonic inhibition exerted by the NPY/AgRP neurons over the anorexigenic POMC/CART neurons. Both of these ultimately enhance appetite [4,17,18]. The ability of ghrelin to increase food intake and body weight is mediated through the stimulation of NPY production in the hypothalamic ARC, where it antagonizes the inhibitory effect on NPY secretion displayed by leptin and insulin [19].The purpose of this chapter is to provide background information on the relationship between the main appetite regulatory peptides NPY and ghrelin, and insulin resistance. The role of NPY and ghrelin in food intake and body weight control in humans, and their ...

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Ghrelin immunoreactivity in human plasma is suppressed by somatostatin

Cited by 127 publications

References 49 publications

Helicobacter pylori has no effect on plasma ghrelin levels

Helicobacter pylori has no effect on plasma ghrelin levels

Estimation of gastric ghrelin-positive cells activity in hyperthyroid rats.

Appetite Regulatory Peptides and Insulin Resistance

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