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Artykuły w czasopismach na temat „Ghrelin signaling”

Autor: Grafiati

Data publikacji: 2 listopada 2024

Data aktualizacji: 31 lipca 2025

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1

Hougland, James L. "Ghrelin octanoylation by ghrelin O-acyltransferase: Unique protein biochemistry underlying metabolic signaling." Biochemical Society Transactions 47, no. 1 (2019): 169–78. http://dx.doi.org/10.1042/bst20180436.

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Abstract Ghrelin is a small peptide hormone that requires a unique post-translational modification, serine octanoylation, to bind and activate the GHS-R1a receptor. Ghrelin signaling is implicated in a variety of neurological and physiological processes, but is most well known for its roles in controlling hunger and metabolic regulation. Ghrelin octanoylation is catalyzed by ghrelin O-acyltransferase (GOAT), a member of the membrane-bound O-acyltransferase (MBOAT) enzyme family. From the status of ghrelin as the only substrate for GOAT in the human genome to the source and requirement for the

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Holst, Birgitte, Erik Brandt, Anders Bach, Anders Heding, and Thue W. Schwartz. "Nonpeptide and Peptide Growth Hormone Secretagogues Act Both as Ghrelin Receptor Agonist and as Positive or Negative Allosteric Modulators of Ghrelin Signaling." Molecular Endocrinology 19, no. 9 (2005): 2400–2411. http://dx.doi.org/10.1210/me.2005-0059.

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Abstract Two nonpeptide (L692,429 and MK-677) and two peptide [GH-releasing peptide (GHRP)-6 and ghrelin] agonists were compared in binding and in signal transduction assays: calcium mobilization, inositol phosphate turnover, cAMP-responsive element (CRE), and serum-responsive element (SRE) controlled transcription, as well as arrestin mobilization. MK-677 acted as a simple agonist having an affinity of 6.5 nm and activated all signal transduction systems with similar high potency (0.2–1.4 nm). L-692,429 also displayed a very similar potency in all signaling assays (25–60 nm) but competed with

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Heldsinger, Andrea, Gintautas Grabauskas, Xiaoyin Wu, et al. "Ghrelin Induces Leptin Resistance by Activation of Suppressor of Cytokine Signaling 3 Expression in Male Rats: Implications in Satiety Regulation." Endocrinology 155, no. 10 (2014): 3956–69. http://dx.doi.org/10.1210/en.2013-2095.

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Abstract The anorexigenic adipocyte-derived hormone leptin and the orexigenic hormone ghrelin act in opposition to regulate feeding behavior via the vagal afferent pathways. The mechanisms by which ghrelin exerts its inhibitory effects on leptin are unknown. We hypothesized that ghrelin activates the exchange protein activated by cAMP (Epac), inducing increased SOCS3 expression, which negatively affects leptin signal transduction and neuronal firing in nodose ganglia (NG) neurons. We showed that 91 ± 3% of leptin receptor (LRb) –bearing neurons contained ghrelin receptors (GHS-R1a) and that gh

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4

Holliday, Nicholas D., Birgitte Holst, Elena A. Rodionova, Thue W. Schwartz, and Helen M. Cox. "Importance of Constitutive Activity and Arrestin-Independent Mechanisms for Intracellular Trafficking of the Ghrelin Receptor." Molecular Endocrinology 21, no. 12 (2007): 3100–3112. http://dx.doi.org/10.1210/me.2007-0254.

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Abstract The ghrelin receptor (GhrelinR) and its related orphan GPR39 each display constitutive signaling, but only GhrelinRs undergo basal internalization. Here we investigate these differences by considering the roles of the C tail receptor domains for constitutive internalization and activity. Furthermore the interaction between phosphorylated receptors and β-arrestin adaptor proteins has been examined. Replacement of the FLAG-tagged GhrelinR C tail with the equivalent GPR39 domain (GhR-39 chimera) preserved Gq signaling. However in contrast to the GhrelinR, GhR-39 receptors exhibited no ba

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5

Wu, Chia-Shan, Jiyeon Noh, Ellie Tuchaai, et al. "SUPPRESSION OF GHRELIN SIGNALING EXACERBATES ULCERATIVE COLITIS IN OLDER MICE." Innovation in Aging 3, Supplement_1 (2019): S87. http://dx.doi.org/10.1093/geroni/igz038.334.

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Abstract The aging process is characterized by increased chronic low-grade inflammation, aka inflamm-aging, which offend is accompanied by ‘leaky gut’ syndrome. Inflamm-aging is a highly significant risk factor for both morbidity and mortality in the older adult population (&gt;65 years of age). In addition, there is a growing prevalence of inflammatory bowel disease (IBD), a chronic inflammatory condition of the gastrointestinal tract in the older adult population. The pathogenesis of late-onset IBD is suggested to be more complex compared with younger IBD patients; the causes determining

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6

Lin, Tsung-Chieh, Yuan-Ming Yeh, Wen-Lang Fan, et al. "Ghrelin Upregulates Oncogenic Aurora A to Promote Renal Cell Carcinoma Invasion." Cancers 11, no. 3 (2019): 303. http://dx.doi.org/10.3390/cancers11030303.

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Ghrelin is a peptide hormone, originally identified from the stomach, that functions as an endogenous ligand of the growth hormone secretagogue receptor (GHSR) and promotes growth hormone (GH) release and food intake. Increasing reports point out ghrelin’s role in cancer progression. We previously characterized ghrelin’s prognostic significance in the clear cell subtype of renal cell carcinoma (ccRCC), and its pro-metastatic ability via Snail-dependent cell migration. However, ghrelin’s activity in promoting cell invasion remains obscure. In this study, an Ingenuity Pathway Analysis (IPA)-base

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7

Madison, Lisa D., Jarrad M. Scarlett, Peter Levasseur, et al. "Prostacyclin signaling regulates circulating ghrelin during acute inflammation." Journal of Endocrinology 196, no. 2 (2007): 263–73. http://dx.doi.org/10.1677/joe-07-0478.

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Ghrelin is an octanoylated 28 amino acid peptide predominantly secreted by the stomach, and has potent stimulatory effects on appetite. Several laboratories, including our own, have demonstrated that ghrelin levels fall in states of acute inflammation brought about by injection of bacterial lipopolysaccharide (LPS). We now demonstrate that the decrease in circulating ghrelin is not due to a decrease in ghrelin gene expression, but is instead likely to be due to an acute decrease in ghrelin secretion. Furthermore, we have found that the change in circulating ghrelin during acute inflammation re

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8

Xu, Geyang, Yin Li, Wenjiao An, et al. "Gastric Mammalian Target of Rapamycin Signaling Regulates Ghrelin Production and Food Intake." Endocrinology 150, no. 8 (2009): 3637–44. http://dx.doi.org/10.1210/en.2009-0372.

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Ghrelin, a gastric hormone, provides a hunger signal to the central nervous system to stimulate food intake. Mammalian target of rapamycin (mTOR) is an intracellular fuel sensor critical for cellular energy homeostasis. Here we showed the reciprocal relationship of gastric mTOR signaling and ghrelin during changes in energy status. mTOR activity was down-regulated, whereas gastric preproghrelin and circulating ghrelin were increased by fasting. In db/db mice, gastric mTOR signaling was enhanced, whereas gastric preproghrelin and circulating ghrelin were decreased. Inhibition of the gastric mTO

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9

Gluck, Elizabeth F., Natalie Stephens, and Steven J. Swoap. "Peripheral ghrelin deepens torpor bouts in mice through the arcuate nucleus neuropeptide Y signaling pathway." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (2006): R1303—R1309. http://dx.doi.org/10.1152/ajpregu.00232.2006.

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Many small mammals have the ability to enter torpor, characterized by a controlled drop in body temperature (Tb). We hypothesized that ghrelin would modulate torpor bouts, because torpor is induced by fasting in mice coincident with elevated circulating ghrelin. Female National Institutes of Health (NIH) Swiss mice were implanted with a Tb telemeter and housed at an ambient temperature (Ta) of 18°C. On fasting, all mice entered a bout of torpor (minimum Tb: 23.8 ± 2.0°C). Peripheral ghrelin administration (100 μg) during fasting significantly deepened the bout of torpor (Tb minimum: 19.4 ± 0.5

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10

Hosoda, Hiroshi. "Effect of Ghrelin on the Cardiovascular System." Biology 11, no. 8 (2022): 1190. http://dx.doi.org/10.3390/biology11081190.

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Ghrelin, an n-octanoyl-modified 28-amino-acid-peptide, was first discovered in the human and rat stomach as an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Ghrelin-GHS-R1a signaling regulates feeding behavior and energy balance, promotes vascular activity and angiogenesis, improves arrhythmia and heart failure, and also protects against cardiovascular disease by suppressing cardiac remodeling after myocardial infarction. Ghrelin’s cardiovascular protective effects are mediated by the suppression of sympathetic activity; activation of parasympathetic activity; allevia

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11

Egecioglu, Emil, Mikael Bjursell, Anna Ljungberg, et al. "Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice." American Journal of Physiology-Endocrinology and Metabolism 290, no. 2 (2006): E317—E325. http://dx.doi.org/10.1152/ajpendo.00181.2005.

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We have previously shown that growth hormone (GH) overexpression in the brain increased food intake, accompanied with increased hypothalamic agouti-related protein (AgRP) expression. Ghrelin, which stimulates both appetite and GH secretion, was injected intracerebroventricularly to GHR−/− and littermate control (+/+) mice to determine whether ghrelin's acute effects on appetite are dependent on GHR signaling. GHR−/− mice were also analyzed with respect to serum levels of lipoproteins, apolipoprotein (apo)B, leptin, glucose, and insulin as well as body composition. Central injection of ghrelin

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12

Liao, Pengzhi, Dan Yang, Duan Liu, and Yuehong Zheng. "GLP-1 and Ghrelin Attenuate High Glucose/High Lipid-Induced Apoptosis and Senescence of Human Microvascular Endothelial Cells." Cellular Physiology and Biochemistry 44, no. 5 (2017): 1842–55. http://dx.doi.org/10.1159/000485820.

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Background/Aims: GLP-1 and ghrelin are common appetite-regulating hormones. Both have multiple functions beyond metabolic regulation. However, the effects of GLP-1 and ghrelin on endothelial biology are not fully understood. Here, we investigate the roles of GLP-1 and ghrelin in microvascular endothelial apoptosis and senescence. Methods: Human microvascular endothelial cells (HMECs) were exposed to high glucose/high lipid (HG/HL) conditions and treated with GLP-1 or ghrelin. Cellular apoptosis, senescence, and mitochondrial function were measured. In addition, the MAPK and Akt signaling pathw

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13

Suzuki, Hajime, Akihiro Asakawa, Namiko Kawamura, Takakazu Yagi, and Akio Inui. "Hesperidin Potentiates Ghrelin Signaling." Recent Patents on Food, Nutrition & Agriculture 6, no. 1 (2014): 60–63. http://dx.doi.org/10.2174/2212798406666140825120623.

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Sustkova-Fiserova, Magdalena, Chrysostomos Charalambous, Anna Khryakova, Alina Certilina, Marek Lapka, and Romana Šlamberová. "The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions." International Journal of Molecular Sciences 23, no. 2 (2022): 761. http://dx.doi.org/10.3390/ijms23020761.

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Drug addiction causes constant serious health, social, and economic burden within the human society. The current drug dependence pharmacotherapies, particularly relapse prevention, remain limited, unsatisfactory, unreliable for opioids and tobacco, and even symptomatic for stimulants and cannabinoids, thus, new more effective treatment strategies are researched. The antagonism of the growth hormone secretagogue receptor type A (GHS-R1A) has been recently proposed as a novel alcohol addiction treatment strategy, and it has been intensively studied in experimental models of other addictive drugs

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15

Rogers, Nicole H., Heidi Walsh, Oscar Alvarez-Garcia, et al. "Metabolic Benefit of Chronic Caloric Restriction and Activation of Hypothalamic AGRP/NPY Neurons in Male Mice Is Independent of Ghrelin." Endocrinology 157, no. 4 (2016): 1430–42. http://dx.doi.org/10.1210/en.2015-1745.

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Abstract Aging is associated with attenuated ghrelin signaling. During aging, chronic caloric restriction (CR) produces health benefits accompanied by enhanced ghrelin production. Ghrelin receptor (GH secretagogue receptor 1a) agonists administered to aging rodents and humans restore the young adult phenotype; therefore, we tested the hypothesis that the metabolic benefits of CR are mediated by endogenous ghrelin. Three month-old male mice lacking ghrelin (Ghrelin−/−) or ghrelin receptor (Ghsr−/−), and their wild-type (WT) littermates were randomly assigned to 2 groups: ad libitum (AL) fed and

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16

McGovern-Gooch, Kayleigh R., Trevor Rodrigues, Joseph E. Darling, Michelle A. Sieburg, Alfonso Abizaid, and James L. Hougland. "Ghrelin Octanoylation Is Completely Stabilized in Biological Samples by Alkyl Fluorophosphonates." Endocrinology 157, no. 11 (2016): 4330–38. http://dx.doi.org/10.1210/en.2016-1657.

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Ghrelin is a peptide hormone involved in multiple physiological processes related to energy homeostasis. This hormone features a unique posttranslational serine octanoylation modification catalyzed by the enzyme ghrelin O-acyltransferase, with serine octanoylation essential for ghrelin to bind and activate its cognate receptor. Ghrelin deacylation rapidly occurs in circulation, with both ghrelin and desacyl ghrelin playing important roles in biological signaling. Understanding the regulation and physiological impact of ghrelin signaling requires the ability to rapidly protect ghrelin from deac

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17

Buckinx, An, Yana Van Den Herrewegen, Anouk Pierre, et al. "Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model." International Journal of Molecular Sciences 20, no. 10 (2019): 2480. http://dx.doi.org/10.3390/ijms20102480.

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The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gαq/11, Gαi/o, Gα12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1

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Skibicka, Karolina P., Rozita H. Shirazi, Caroline Hansson, and Suzanne L. Dickson. "Ghrelin Interacts with Neuropeptide Y Y1 and Opioid Receptors to Increase Food Reward." Endocrinology 153, no. 3 (2012): 1194–205. http://dx.doi.org/10.1210/en.2011-1606.

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Ghrelin, a stomach-derived hormone, is an orexigenic peptide that was recently shown to potently increase food reward behavior. The neurochemical circuitry that links ghrelin to the mesolimbic system and food reward behavior remains unclear. Here we examined the contribution of neuropeptide Y (NPY) and opioids to ghrelin's effects on food motivation and intake. Both systems have well-established links to the mesolimbic ventral tegmental area (VTA) and reward/motivation control. NPY mediates the effect of ghrelin on food intake via activation of NPY-Y1 receptor (NPY-Y1R); their connection with

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Bagnasco, Michela, Pushpa S. Kalra, and Satya P. Kalra. "Ghrelin and Leptin Pulse Discharge in Fed and Fasted Rats." Endocrinology 143, no. 2 (2002): 726–29. http://dx.doi.org/10.1210/endo.143.2.8743.

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Abstract Ghrelin stimulates and leptin inhibits appetite by modulating neuropeptide Y (NPY) signaling in the hypothalamus. Analysis of plasma ghrelin and leptin by sensitive radioimmunoassays showed that the two peripheral hormones are secreted in pulsatile fashion in rats consuming ad libitum rat chow. Fasting augmented all parameters of ghrelin pulsatile secretion and diminished leptin secretion by selectively attenuating the pulse amplitude; concomitantly it produced synchrony in ghrelin and leptin pulse discharge. These studies imply that a synchronous leptin restraint and ghrelin stimulus

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Chung, Hyunju, Endan Li, Yumi Kim, Sehee Kim, and Seungjoon Park. "Multiple signaling pathways mediate ghrelin-induced proliferation of hippocampal neural stem cells." Journal of Endocrinology 218, no. 1 (2013): 49–59. http://dx.doi.org/10.1530/joe-13-0045.

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Ghrelin, an endogenous ligand for the GH secretagogue receptor (GHS-R) receptor 1a (GHS-R1a), has been implicated in several physiologic processes involving the hippocampus. The aim of this study was to investigate the molecular mechanisms of ghrelin-stimulated neurogenesis using cultured adult rat hippocampal neural stem cells (NSCs). The expression of GHS-R1a was detected in hippocampal NSCs, as assessed by western blot analysis and immunocytochemistry. Ghrelin treatment increased the proliferation of cultured hippocampal NSCs assessed by BrdU incorporation. The exposure of cells to the rece

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Gong, Zhi, Makoto Yoshimura, Sayaka Aizawa, et al. "G protein-coupled receptor 120 signaling regulates ghrelin secretion in vivo and in vitro." American Journal of Physiology-Endocrinology and Metabolism 306, no. 1 (2014): E28—E35. http://dx.doi.org/10.1152/ajpendo.00306.2013.

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Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is produced predominantly in the stomach. It has been reported that endogenous ghrelin levels are increased by fasting and decreased immediately after feeding and that fasting-induced ghrelin release is controlled by the sympathetic nervous system. However, the mechanisms of plasma ghrelin decrement after feeding are poorly understood. Here, we studied the control of ghrelin secretion using ghrelin-producing cell lines and found that these cells express high levels of mRNA encoding G-protein coupled receptor 120 (GPR12

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22

Amitani, Marie, Haruka Amitani, Kai-Chun Cheng, et al. "The Role of Ghrelin and Ghrelin Signaling in Aging." International Journal of Molecular Sciences 18, no. 7 (2017): 1511. http://dx.doi.org/10.3390/ijms18071511.

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Naznin, Farhana, Koji Toshinai, T. M. Zaved Waise, Tadashi Okada, Hideyuki Sakoda, and Masamitsu Nakazato. "Restoration of metabolic inflammation-related ghrelin resistance by weight loss." Journal of Molecular Endocrinology 60, no. 2 (2018): 109–18. http://dx.doi.org/10.1530/jme-17-0192.

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High-fat diet (HFD)-induced metabolic inflammation in the central and peripheral organs contributes to the pathogenesis of obesity. Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammation. This study was undertaken to investigate whether ghrelin resistance is associated with progressive development of metabolic inflammation. In mice, ghrelin’s orexigenic activity was abolished 2–4 weeks after the commencement of HFD (60% of energy from fat), consistent with the timing of accumulati

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Nahata, Miwa, Shuichi Muto, Nobuhiko Oridate, et al. "Impaired ghrelin signaling is associated with gastrointestinal dysmotility in rats with gastroesophageal reflux disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 1 (2012): G42—G53. http://dx.doi.org/10.1152/ajpgi.00462.2011.

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Gastroesophageal reflux disease (GERD) is often associated with decreased upper gastrointestinal motility, and ghrelin is an appetite-stimulating hormone known to increase gastrointestinal motility. We investigated whether ghrelin signaling is impaired in rats with GERD and studied its involvement in upper gastrointestinal motility. GERD was induced surgically in Wistar rats. Rats were injected intravenously with ghrelin (3 nmol/rat), after which gastric emptying, food intake, gastroduodenal motility, and growth hormone (GH) release were investigated. Furthermore, plasma ghrelin levels and the

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Ma, Liangxiao, Hong Tang, Yue Yin, et al. "HDAC5-mTORC1 Interaction in Differential Regulation of Ghrelin and Nucleobindin 2 (NUCB2)/Nesfatin-1." Molecular Endocrinology 29, no. 11 (2015): 1571–80. http://dx.doi.org/10.1210/me.2015-1184.

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Abstract Sodium valporate (VPA), a broad-spectrum inhibitor of histone deacetylases (HDACs), increased ghrelin whereas decreased nesfatin-1 in mice fed normal chow diet or high-fat diet. Alterations in ghrelin and nucleobindin 2/nesfatin-1 were mediated by HDAC5 but not HDAC4. Activation of mTORC1 significantly attenuated the effect of VPA on ghrelin and nesfatin-1 levels. HDAC5 coimmunoprecipitated with raptor. Inhibition of HDAC5 by VPA, trichostatin A, or siHDAC5 markedly increased acetylation of raptor Lys840 and subsequent phosphorylation of raptor Ser792, resulting in suppression of mTOR

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Katare, Rajesh, Shruti Rawal, Pujika Emani Munasinghe, et al. "Ghrelin Promotes Functional Angiogenesis in a Mouse Model of Critical Limb Ischemia Through Activation of Proangiogenic MicroRNAs." Endocrinology 157, no. 2 (2015): 432–45. http://dx.doi.org/10.1210/en.2015-1799.

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Abstract Current therapeutic strategies for the treatment of critical limb ischemia (CLI) have only limited success. Recent in vitro evidence in the literature, using cell lines, proposes that the peptide hormone ghrelin may have angiogenic properties. In this study, we aim to investigate if ghrelin could promote postischemic angiogenesis in a mouse model of CLI and, further, identify the mechanistic pathway(s) that underpin ghrelin's proangiogenic properties. CLI was induced in male CD1 mice by femoral artery ligation. Animals were then randomized to receive either vehicle or acylated ghrelin

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Li, Danjie, Shaojian Li, Qinling Pan, et al. "Gastric Mammalian Target of Rapamycin Signaling Contributes to Inhibition of Ghrelin Expression Induced by Roux-En-Y Gastric Bypass." Cellular Physiology and Biochemistry 51, no. 2 (2018): 664–80. http://dx.doi.org/10.1159/000495325.

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Background/Aims: Roux-en-Y Gastric Bypass, RYGB, is the most effective strategy to control body weight in morbid obesity. RYGB leads to rapid improvement of glycemic status and weight loss, which are largely attributed to the alteration of gastrointestinal hormones including ghrelin. The current study examined potential mechanisms of altered ghrelin synthesis after RYGB. Methods: Gastric mammalian target of rapamycin (mTOR) signaling, ghrelin synthesis and secretion were determined in lean or obese male mice with or without RYGB operation, as well as in obese patients pre- and post-RYGB surger

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Wang, Qin, Ming Zheng, Yue Yin та Weizhen Zhang. "Ghrelin Stimulates Hepatocyte Proliferation via Regulating Cell Cycle Through GSK3β/Β-Catenin Signaling Pathway". Cellular Physiology and Biochemistry 50, № 5 (2018): 1698–710. http://dx.doi.org/10.1159/000494789.

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Background/Aims: Obesity is associated with a reduction in ghrelin, a 28 aa gastric hormone. Whether reduced ghrelin contributes to the impaired proliferation of hepatocytes associated with obesity-related steatosis remains largely unknown. Here we examined the effects of ghrelin on the proliferation of hepatocytes derived from lean and obese mice. Methods: AML 12 cells or hepatocytes isolated from mice fed normal chow diet (NCD) or high fat diet (HFD) were used. Effects of ghrelin on hepatocyte proliferation were detected with CCK8 assay and EdU staining. Cell cycle was analyzed by flow cytom

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Naznin, Farhana, Koji Toshinai, T. M. Zaved Waise, et al. "Diet-induced obesity causes peripheral and central ghrelin resistance by promoting inflammation." Journal of Endocrinology 226, no. 1 (2015): 81–92. http://dx.doi.org/10.1530/joe-15-0139.

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Ghrelin, a stomach-derived orexigenic peptide, transmits starvation signals to the hypothalamus via the vagus afferent nerve. Peripheral administration of ghrelin does not induce food intake in high fat diet (HFD)-induced obese mice. We investigated whether this ghrelin resistance was caused by dysfunction of the vagus afferent pathway. Administration (s.c.) of ghrelin did not induce food intake, suppression of oxygen consumption, electrical activity of the vagal afferent nerve, phosphorylation of ERK2 and AMP-activated protein kinase alpha in the nodose ganglion, or Fos expression in hypothal

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Holst, Birgitte, Adam Cygankiewicz, Tine Halkjær Jensen, Michael Ankersen, and Thue W. Schwartz. "High Constitutive Signaling of the Ghrelin Receptor—Identification of a Potent Inverse Agonist." Molecular Endocrinology 17, no. 11 (2003): 2201–10. http://dx.doi.org/10.1210/me.2003-0069.

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Abstract Ghrelin is a GH-releasing peptide that also has an important role as an orexigenic hormone-stimulating food intake. By measuring inositol phosphate turnover or by using a reporter assay for transcriptional activity controlled by cAMP-responsive elements, the ghrelin receptor showed strong, ligand-independent signaling in transfected COS-7 or human embryonic kidney 293 cells. Ghrelin and a number of the known nonpeptide GH secretagogues acted as agonists stimulating inositol phosphate turnover further. In contrast, the low potency ghrelin antagonist, [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-subs

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Zhang, Chengshuo, Le Li, Bochao Zhao, et al. "Ghrelin Protects against Dexamethasone-Induced INS-1 Cell Apoptosis via ERK and p38MAPK Signaling." International Journal of Endocrinology 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/4513051.

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Glucocorticoid excess induces apoptosis of islet cells, which may result in diabetes. In this study, we investigated the protective effect of ghrelin on dexamethasone-induced INS-1 cell apoptosis. Our data showed that ghrelin (0.1 μM) inhibited dexamethasone-induced (0.1 μM) apoptosis of INS-1 cells and facilitated cell proliferation. Moreover, ghrelin upregulated Bcl-2 expression, downregulated Bax expression, and decreased caspase-3 activity. The protective effect of ghrelin against dexamethasone-induced INS-1 cell apoptosis was mediated via growth hormone secretagogue receptor 1a. Further s

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Currie, Paul J., Aaisha Mirza, Rebecca Fuld, Diana Park, and Joseph R. Vasselli. "Ghrelin is an orexigenic and metabolic signaling peptide in the arcuate and paraventricular nuclei." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (2005): R353—R358. http://dx.doi.org/10.1152/ajpregu.00756.2004.

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Ghrelin is a 28-amino acid acylated peptide and is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). The GHS-R is expressed in hypothalamic nuclei, including the arcuate nucleus (Arc) where it is colocalized with neuropeptide Y (NPY) neurons. In the present study, we examined the effects of ghrelin on feeding and energy substrate utilization (respiratory quotient; RQ) following direct injections into either the arcuate or the paraventricular nucleus (PVN) of the hypothalamus. Ghrelin was administered at the beginning of the dark cycle at doses of 15–60 pmol to male an

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Lee, Junho. "Ghrelin stimulates cell proliferation in T cells (109.22)." Journal of Immunology 186, no. 1_Supplement (2011): 109.22. http://dx.doi.org/10.4049/jimmunol.186.supp.109.22.

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Abstract Ghrelin is a 28 amino acid acylated peptide, which is produced and secreted by X/A-like enteroendocrine cells of the stomach. We have recently demonstrated that ghrelin is expressed by various immune cells including T- and B-lymphocytes, monocytes and neutrophils. These immune cells have also been shown to express the ghrelin receptor, namely the growth hormone secretagogue receptor (GHS-R). In the present study, we have investigated the effects of ghrelin on T cell proliferation and its signaling through its cell surface receptor. We have found that ghrelin induces a modest increase

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Koyama, Hiroyuki, Hiroshi Iwakura, Katsuko Dote, et al. "Comprehensive Profiling of GPCR Expression in Ghrelin-Producing Cells." Endocrinology 157, no. 2 (2015): 692–704. http://dx.doi.org/10.1210/en.2015-1784.

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Abstract To determine the comprehensive G protein-coupled receptor (GPCR) expression profile in ghrelin-producing cells and to elucidate the role of GPCR-mediated signaling in the regulation of ghrelin secretion, we determined GPCR expression profiles by RNA sequencing in the ghrelin-producing cell line MGN3-1 and analyzed the effects of ligands for highly expressed receptors on intracellular signaling and ghrelin secretion. Expression of selected GPCRs was confirmed in fluorescence-activated cell-sorted fluorescently tagged ghrelin-producing cells from ghrelin-promoter CreERT2/Rosa-CAG-LSL-Zs

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Xu, Xiangbin, Bong Sook Jhun, Chang Hoon Ha, and Zheng-Gen Jin. "Molecular Mechanisms of Ghrelin-Mediated Endothelial Nitric Oxide Synthase Activation." Endocrinology 149, no. 8 (2008): 4183–92. http://dx.doi.org/10.1210/en.2008-0255.

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Metabolic syndrome accelerates the atherosclerotic process, and the earliest event of which is endothelial dysfunction. Ghrelin, a newly discovered gastric peptide, improves endothelial function and inhibits proatherogenic changes. In particular, low ghrelin concentration has been associated with several features of metabolic syndrome, including obesity, insulin resistance, and high blood pressure. However, the molecular mechanisms underlying ghrelin vascular actions remain largely unclear. Here, we showed that ghrelin activated endothelial nitric oxide (NO) synthase (eNOS) in cultured endothe

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Ma, Xiaojun, Yuezhen Lin, Ligen Lin, et al. "Ablation of ghrelin receptor in leptin-deficient ob/ob mice has paradoxical effects on glucose homeostasis when compared with ablation of ghrelin in ob/ob mice." American Journal of Physiology-Endocrinology and Metabolism 303, no. 3 (2012): E422—E431. http://dx.doi.org/10.1152/ajpendo.00576.2011.

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The orexigenic hormone ghrelin is important in diabetes because it has an inhibitory effect on insulin secretion. Ghrelin ablation in leptin-deficient ob/ob ( Ghrelin−/−: ob/ ob) mice increases insulin secretion and improves hyperglycemia. The physiologically relevant ghrelin receptor is the growth hormone secretagogue receptor (GHS-R), and GHS-R antagonists are thought to be an effective strategy for treating diabetes. However, since some of ghrelin's effects are independent of GHS-R, we have utilized genetic approaches to determine whether ghrelin's effect on insulin secretion is mediated th

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Overduin, Joost, Dianne P. Figlewicz, Jennifer Bennett-Jay, Sepideh Kittleson, and David E. Cummings. "Ghrelin increases the motivation to eat, but does not alter food palatability." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 3 (2012): R259—R269. http://dx.doi.org/10.1152/ajpregu.00488.2011.

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Homeostatic eating cannot explain overconsumption of food and pathological weight gain. A more likely factor promoting excessive eating is food reward and its representation in the central nervous system (CNS). The anorectic hormones leptin and insulin reduce food reward and inhibit related CNS reward pathways. Conversely, the orexigenic gastrointestinal hormone ghrelin activates both homeostatic and reward-related neurocircuits. The current studies were conducted to identify in rats the effects of intracerebroventricular ghrelin infusions on two distinct aspects of food reward: hedonic valuat

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Petersen, Pia Steen, David P. D. Woldbye, Andreas Nygaard Madsen, et al. "In Vivo Characterization of High Basal Signaling from the Ghrelin Receptor." Endocrinology 150, no. 11 (2009): 4920–30. http://dx.doi.org/10.1210/en.2008-1638.

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The receptor for the orexigenic peptide, ghrelin, is one of the most constitutively active 7TM receptors known, as demonstrated under in vitro conditions. Change in expression of a constitutively active receptor is associated with change in signaling independent of the endogenous ligand. In the following study, we found that the expression of the ghrelin receptor in the hypothalamus was up-regulated approximately 2-fold in rats both during 48-h fasting and by streptozotocin-induced hyperphagia. In a separate experiment, to probe for the effect of the high basal signaling of the ghrelin recepto

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Schalla, Martha, and Andreas Stengel. "The Role of Ghrelin in Anorexia Nervosa." International Journal of Molecular Sciences 19, no. 7 (2018): 2117. http://dx.doi.org/10.3390/ijms19072117.

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Ghrelin, a 28-amino acid peptide hormone expressed in X/A-like endocrine cells of the stomach, is the only known peripherally produced and centrally acting peptide that stimulates food intake and therefore attracted a lot of attention with one major focus on the treatment of conditions where an increased energy intake or body weight gain is desired. Anorexia nervosa is an eating disorder characterized by a pronounced reduction of body weight, a disturbed body image and hormonal alterations. Ghrelin signaling has been thoroughly investigated under conditions of anorexia nervosa. The present rev

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Wang, Jun, Lin He, Bahetiyaer Huwatibieke, et al. "Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway." International Journal of Molecular Sciences 19, no. 9 (2018): 2530. http://dx.doi.org/10.3390/ijms19092530.

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Adipose tissue is hyper-vascularized. Vessels in adipose tissue not only supply nutrients and oxygen to nourish adipocytes, but also provide cytokines that regulate mass and function of adipose tissue. Understanding the fundamental mechanisms how vessels modulate adipocyte functions would provide new therapeutic options for treatment of metabolic disease and obesity. In recent years, researches about ghrelin are focused on glucose and lipid metabolism, but its effect on vascular function remains uncharacterized. In the present study, ghrelin receptor gene deletion mice (Ghsr−/− mice) were used

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Urai, Hidenori, Tatsuhiko Azegami, Motoaki Komatsu, et al. "Ghrelin Promotes Lipid Uptake into White Adipose Tissue via Endothelial Growth Hormone Secretagogue-Receptor in Mice." Nutrients 17, no. 1 (2024): 146. https://doi.org/10.3390/nu17010146.

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Background/Objectives: Endothelial peroxisome proliferator-activated receptor gamma (PPARγ) regulates adipose tissue by facilitating lipid uptake into white adipocytes, but the role of endothelial lipid transport in systemic energy balance remains unclear. Ghrelin conveys nutritional information through the central nervous system and increases adiposity, while deficiency in its receptor, growth hormone secretagogue-receptor (GHSR), suppresses adiposity on a high-fat diet. This study aims to examine the effect of ghrelin/GHSR signaling in the endothelium on lipid metabolism. Methods: We compare

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Wang, Chia-Hao, Ching-Yu Tseng, Wei-Li Hsu, and Jason T. C. Tzen. "Establishment of a Cell Line Stably Expressing the Growth Hormone Secretagogue Receptor to Identify Crocin as a Ghrelin Agonist." Biomolecules 12, no. 12 (2022): 1813. http://dx.doi.org/10.3390/biom12121813.

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The growth hormone secretagogue receptor-1a (GHSR1a) is the endogenous receptor for ghrelin. Activation of GHSR1a participates in many physiological processes including energy homeostasis and eating behavior. Due to its transitory half-life, the efficacy of ghrelin treatment in patients is restricted; hence the development of new adjuvant therapy is an urgent need. This study aimed to establish a cell line stably expressing GHSR1a, which could be employed to screen potential ghrelin agonists from natural compounds. First, by means of lentiviral transduction, the genome of a human HEK293T cell

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Howell, Erin, Hannah Baumgartner, Lia Zallar, Joaquín Selva, Liv Engel, and Paul Currie. "Glucagon-Like Peptide-1 (GLP-1) and 5-Hydroxytryptamine 2c (5-HT2c) Receptor Agonists in the Ventral Tegmental Area (VTA) Inhibit Ghrelin-Stimulated Appetitive Reward." International Journal of Molecular Sciences 20, no. 4 (2019): 889. http://dx.doi.org/10.3390/ijms20040889.

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Current literature indicates that the orexigenic peptide ghrelin increases appetitive motivation via signaling in the mesolimbic reward system. Another gastric peptide, glucagon-like peptide-1 (GLP-1), and the neurotransmitter 5-hydroxytryptamine (5-HT), are both known to suppress operant responding for food by acting on key mesolimbic nuclei, including the ventral tegmental area (VTA). In order to investigate the interaction effects of ghrelin, GLP-1, and 5-HT within the VTA, we measured operant responding for sucrose pellets after the administration of ghrelin, the GLP-1 receptor agonist exe

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Rouault, Alix A. J., Luciana K. Rosselli-Murai, Ciria C. Hernandez, Luis E. Gimenez, Gregory G. Tall, and Julien A. Sebag. "The GPCR accessory protein MRAP2 regulates both biased signaling and constitutive activity of the ghrelin receptor GHSR1a." Science Signaling 13, no. 613 (2020): eaax4569. http://dx.doi.org/10.1126/scisignal.aax4569.

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Ghrelin is a hormone secreted by the stomach during fasting periods and acts through its receptor, the growth hormone secretagogue 1a (GHSR1a), to promote food intake and prevent hypoglycemia. As such, GHSR1a is an important regulator of energy and glucose homeostasis and a target for the treatment of obesity. Here, we showed that the accessory protein MRAP2 altered GHSR1a signaling by inhibiting its constitutive activity, as well as by enhancing its G protein–dependent signaling and blocking the recruitment and signaling of β-arrestin in response to ghrelin. In addition, the effects of MRAP2

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Mineev, V. N., T. M. Lalaeva, and A. A. Lebedeva. "Ghrelin signaling pathway in bronchial asthma." Russian Pulmonology 26, no. 1 (2016): 92–97. http://dx.doi.org/10.18093/0869-0189-2016-26-1-92-97.

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Taherkhani, Shokoufeh, Fatemeh Moradi, Masoumeh Hosseini, Mohsen Alipour, and Hadi Feizi. "Homeobox B4 gene expression is upregulated by ghrelin through PI3-kinase signaling pathway in rat’s bone marrow stromal cells." Endocrine Regulations 53, no. 2 (2019): 65–70. http://dx.doi.org/10.2478/enr-2019-0008.

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AbstractObjective. Ghrelin, a 28 amino acid peptide, has diverse physiological roles. Phosphatidylino-sitol-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) are involved in some of the recognized actions of ghrelin. It has been shown that ghrelin upregulates HOXB4 gene expression but the real mechanism of this effect is not clear.Methods. Rat bone marrow stromal cells (BMSCs) were cultured in DMEM. BMSCs were treated with ghrelin (100 μM) for 48 h. Real-time PCR for HOXB4 was performed from Control (untreated BMSCs), BG (BMSCs treated with 100 µM ghrelin), PD (BMSCs tre

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Zheng, Haichong, Wenjie Liang, Wanmei He та ін. "Ghrelin attenuates sepsis-induced acute lung injury by inhibiting the NF-κB, iNOS, and Akt signaling in alveolar macrophages". American Journal of Physiology-Lung Cellular and Molecular Physiology 317, № 3 (2019): L381—L391. http://dx.doi.org/10.1152/ajplung.00253.2018.

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Ghrelin has proven to be protective against sepsis-induced acute lung injury (ALI) via anti-inflammatory effects. However, its mechanisms remain poorly understood. Alveolar macrophages (AMs) play a key role in mediating inflammatory responses during sepsis-induced ALI by secretion of cytokines and chemokines. This study was undertaken to investigate whether ghrelin suppresses inflammatory effects of AMs and therefore may help to attenuate sepsis-induced ALI. A sepsis model in rats was achieved using cecal ligation and puncture. Ghrelin treatment markedly improved histopathological changes in t

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Wagner, Clemens, S. Roy Caplan, and Gloria S. Tannenbaum. "Interactions of ghrelin signaling pathways with the GH neuroendocrine axis: a new and experimentally tested model." Journal of Molecular Endocrinology 43, no. 3 (2009): 105–19. http://dx.doi.org/10.1677/jme-09-0023.

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Growth hormone (GH) is secreted in a pulsatile fashion from the pituitary gland into the circulation. Release is governed by two hypothalamic neuropeptides, growth hormone-releasing hormone (GHRH) and somatostatin (SRIF), resulting in secretion episodes with a periodicity of 3.3 h in the male rat. Ghrelin is an additional recently identified potent GH-secretagogue. However, its in vivo interactions with the GH neuroendocrine axis remain to be elucidated. Moreover, two different sites of ghrelin synthesis are involved, the stomach and the hypothalamus. We used our previously developed core mode

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Jiang, Hong, Lorena Betancourt, and Roy G. Smith. "Ghrelin Amplifies Dopamine Signaling by Cross Talk Involving Formation of Growth Hormone Secretagogue Receptor/Dopamine Receptor Subtype 1 Heterodimers." Molecular Endocrinology 20, no. 8 (2006): 1772–85. http://dx.doi.org/10.1210/me.2005-0084.

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Abstract Our objective is to determine the neuromodulatory role of ghrelin in the brain. To identify neurons that express the ghrelin receptor [GH secretagogue receptor (GHS-R)], we generated GHS-R-IRES-tauGFP mice by gene targeting. Neurons expressing the GHS-R exhibit green fluorescence and are clearly evident in the hypothalamus, hippocampus, cortex, and midbrain. Using immunohistochemistry in combination with green fluorescent protein fluorescence, we identified neurons that coexpress the dopamine receptor subtype 1 (D1R) and GHS-R. The potential physiological relevance of coexpression of

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Iantorno, Micaela, Hui Chen, Jeong-a. Kim, et al. "Ghrelin has novel vascular actions that mimic PI 3-kinase-dependent actions of insulin to stimulate production of NO from endothelial cells." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (2007): E756—E764. http://dx.doi.org/10.1152/ajpendo.00570.2006.

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Ghrelin is an orexigenic peptide hormone secreted by the stomach. In patients with metabolic syndrome and low ghrelin levels, intra-arterial ghrelin administration acutely improves their endothelial dysfunction. Therefore, we hypothesized that ghrelin activates endothelial nitric oxide synthase (eNOS) in vascular endothelium, resulting in increased production of nitric oxide (NO) using signaling pathways shared in common with the insulin receptor. Similar to insulin, ghrelin acutely stimulated increased production of NO in bovine aortic endothelial cells (BAEC) in primary culture (assessed usi

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