Ghrelin
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Ghrelin (pronounced /ˈɡrɛlɪn/), the "hunger hormone", also known as lenomorelin (INN), is a peptide hormone produced by ghrelinergic cells in the gastrointestinal tract[1][2] that functions as a neuropeptide in the central nervous system.[3] Besides regulating appetite, ghrelin also plays a significant role in regulating the distribution and rate of use of energy.[4]
When the stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops.a It acts on hypothalamic brain cells both to increase hunger, and to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake.[5]
The receptor for ghrelin, the ghrelin/growth hormone secretagogue receptor (GHS-R), is found on the same cells in the brain as the receptor for leptin, the satiety hormone that has opposite effects from ghrelin.[6] Ghrelin also plays an important role in regulating reward perception in dopamine neurons that link the ventral tegmental area to the nucleus accumbens[7][8] (a site that plays a role in processing sexual desire, reward, and reinforcement, and in developing addictions) through its colocalized receptors and interaction with dopamine and acetylcholine.[3][9] Ghrelin is encoded by the GHRL gene and is presumably produced from the cleavage of the prepropeptide ghrelin/obestatin. Full-length preproghrelin is homologous to promotilin and both are members of the motilin family.
Unlike the case of many other endogenous peptides, ghrelin is able to cross the blood-brain-barrier, giving exogenously-administered ghrelin unique clinical potential.[10]
1 History and name
2 Gene, transcription products, and structure
3 Ghrelin cells
3.1 Alternative names
4 Function and mechanism of action
5 Blood levels
6 Ghrelin receptor
7 Locations of action
7.1 Gastrointestinal tract
7.2 Pancreas
7.3 Glucose metabolism
7.4 Nervous system
7.4.1 Learning and memory
7.4.2 Depression
7.4.3 Sleep duration
7.4.4 Stress-induced fear
7.4.5 Substantia nigra function
7.5 Reproductive system
7.6 Fetus and neonate
8 Anorexia and obesity
9 Disease management
9.1 Gastric bypass surgery
10 Aging
11 Future clinical uses
History and name
Ghrelin was discovered after the ghrelin receptor (called growth hormone secretagogue type 1A receptor or GHS-R) was discovered in 1996[11] and was reported in 1999.[12] The hormone name is based on its role as a growth hormone-releasing peptide, with reference to the Proto-Indo-European root gʰre-, meaning "to grow".[13]
Gene, transcription products, and structure
File:Preproghrelin 1P7X.png
Preproghrelin (green and blue) and ghrelin (green).
The GHRL gene produces mRNA which has four exons. Five products arise: the first is the 117-amino acid preproghrelin. (It is homologous to promotilin; both are members of the motilin family). It is cleaved to produce proghrelin which is cleaved to produce a 28-amino acid ghrelin (unacylated) and C-ghrelin(acylated). Obestatin is presumed to be cleaved from C-ghrelin.[14]
Ghrelin only becomes active when caprylic (octanoic) acid is linked posttranslationally to serine at the 3-position by the enzyme ghrelin O-acyltransferase (GOAT). It is located on the cell membrane of ghrelin cells in the stomach and pancreas.[15] The non-octanoylated form is desacyl ghrelin. It does not activate the GHS-R receptor but does have other effects: cardiac,[16] anti-ghrelin,[17] appetite stimulation,[18] and inhibition of hepatic glucose output[19] Side-chains other than octanoyl have also been observed: these can also trigger the ghrelin receptor.[20] In particular, decanoyl ghrelin has been found to constitute a significant portion of circulating ghrelin in mice, but as of 2011 its presence in humans has not been established.[21]
Ghrelin cells
The ghrelin cell is also known as an A-like cell (pancreas), X-cell (for unknown function), X/A-like cell (rats), Epsilon cell (pancreas), P/D sub 1 cell (humans) and Gr cell (abbreviation for ghrelin cell).[22]
Ghrelin cells are found mainly in the stomach[23] and duodenum, but also in the jejunum, lungs, pancreatic islets,[24] gonads, adrenal cortex, placenta, and kidney. It has recently been shown that ghrelin is produced locally in the brain[25]
Ghrelin cells are found in oxyntic glands (20% of cells),[26] pyloric glands, and small intestine. They are ovoid cells with granules.[27] They have gastrin receptors.[28] Some produce nesfatin-1.[29] Ghrelin cells are not terminally differentiated in the pancreas: they are progenitor cells that can give rise to A-cells, PP cells and Beta-cells there.[30]
Function and mechanism of action
Ghrelin is a participant in regulating the complex process of energy homeostasis which adjusts both energy input – by adjusting hunger signals – and energy output – by adjusting the proportion of energy going to ATP production, fat storage, glycogen storage, and short-term heat loss. The net result of these processes is reflected in body weight, and is under continuous monitoring and adjustment based on metabolic signals and needs. At any given moment in time, it may be in equilibrium or disequilibrium. Gastric-brain communication is an essential part of energy homeostasis, and several communication pathways are probable, including the gastric intracellular mTOR/S6K1 pathway mediating the interaction among ghrelin, nesfatin and endocannabinoid gastric systems,[31] and both afferent and efferent vagal signals.
Ghrelin and synthetic ghrelin mimetics (growth hormone secretagogues) increase body weight and fat mass[32][33][34] by triggering receptors in the arcuate nucleus[35][36] that include the orexigenic neuropeptide Y (NPY) and agouti-related protein (AgRP) neurons.[37][38] Ghrelin-responsiveness of these neurons is both leptin- and insulin-sensitive.[39] Ghrelin reduces the mechanosensitivity of gastric vagal afferents, so they are less sensitive to gastric distension.[40]
In addition to its function in energy homeostasis, ghrelin also activates the cholinergic–dopaminergic reward link in inputs to the ventral tegmental area and in the mesolimbic pathway,[7] a circuit that communicates the hedonic and reinforcing aspects of natural rewards,[3] such as food and addictive drugs such as ethanol.[39][41][42] Ghrelin receptors are located on neurons in this circuit.[3][8] Hypothalamic ghrelin signalling is required for reward from alcohol[43] and palatable/rewarding foods.[44][45]
Ghrelin has been linked to inducing appetite and feeding behaviors. Circulating ghrelin levels are the highest right before a meal and the lowest right after.[46][47] Injections of ghrelin in both humans and rats have been shown to increase food intake in a dose-dependent manner.[48] So the more ghrelin that is injected the more food that is consumed. However, ghrelin does not increase meal size, only meal number.[49] Ghrelin injections also increase an animal's motivation to seek out food, behaviors including increased sniffing, foraging for food, and hoarding food. Body weight is regulated through energy balance, the amount of energy taken in versus the amount of energy expended over an extended period of time. Studies have shown that ghrelin levels are negatively correlated with weight. This data suggests that ghrelin functions as an adiposity signal, a messenger between the body's energy stores and the brain.[5]
Blood levels
Blood levels are in the pmol/l range. Both active and total ghrelin can be measured.[50] Circulating ghrelin concentrations rise before eating and fall afterward,[46] more strongly in response to protein and carbohydrate than to lipids.[21]
Ghrelin receptor
The ghrelin receptor GHS-R1a (a splice-variant of the growth hormone secretagogue receptor, with the GHS-R1b splice being inactive) is involved in mediating a wide variety of biological effects of ghrelin, including: stimulation of growth hormone release, increase in hunger, modulation of glucose and lipid metabolism, regulation of gastrointestinal motility and secretion, protection of neuronal and cardiovascular cells, and regulation of immune function.[51] They are present in high density in the hypothalamus and pituitary, on the vagus nerve (on both afferent cell bodies and afferent nerve endings) and throughout the gastrointestinal tract.[15][40]
Locations of action
Ghrelin promotes intestinal cell proliferation and inhibits apoptosis during inflammatory states and oxidative stress.[52][53] It also suppresses pro-inflammatory mechanisms and augments anti-inflammatory mechanisms, thus creating a possibility of its therapeutic use in various gastrointestinal inflammatory conditions, including colitis, ischemia reperfusion injury, and sepsis.[54][55] Animal models of colitis, ischemia reperfusion, and sepsis-related gut dysfunction have been shown to benefit from therapeutic doses of ghrelin.[54][55] It has also been shown to have regenerative capacity and is beneficial in mucosal injury to the stomach.[56]
Ghrelin promotes gastrointestinal and pancreatic malignancy.[57][58][59]
Ghrelin inhibits glucose-stimulated insulin secretion from beta cells in the pancreatic islets. Ghrelin does this indirectly by promoting local negative feedback mediated by somatostatin from pancreatic delta cells, which selectively express the ghrelin receptor.[60]
The entire ghrelin system (dAG, AG, GHS-R and GOAT) has a gluco-regulatory action.[61]
The hippocampus plays a significant role in neurotrophy: the cognitive adaptation to changing environments and the process of learning[62][63] and it is a potent stimulator of growth hormone.[12] Animal models indicate that ghrelin may enter the hippocampus from the bloodstream, altering nerve-cell connections, and so altering learning and memory.[64] It is suggested that learning may be best during the day and when the stomach is empty, since ghrelin levels are higher at these times. A similar effect on human memory performance is possible.[62] In rodents, X/A-like cells produce ghrelin.[65]
Ghrelin knock-out mice (who never express ghrelin) have increased anxiety in response to a variety of stressors, such as acute restraint stress and social stress in experimental settings.[66] In normal mice, ghrelin can stimulate the hypothalamic-pituitary-adrenal axis, from the anterior pituitary.[66]
Ghrelin has been shown to have implications for depression prevention. Antidepressant-like attributes were demonstrated when mice with high levels of ghrelin and mice with the ghrelin gene knocked out underwent social defeat stress and then were placed in the forced swim tank. Mice with elevated ghrelin swam more than ghrelin deficient mice.[67] These ghrelin-deficient mice exhibited more social avoidance as well. These mice did not exhibit depression-like behaviors when injected with a commonly prescribed antidepressant, suggesting that ghrelin acts as a short-term natural adaptation against depression.
Sleep duration
Short sleep duration is associated with high levels of ghrelin and obesity. An inverse relationship between the hours of sleep and blood plasma concentrations of ghrelin exists; as the hours of sleep increase, ghrelin levels trend lower and obesity is less likely.[68]
Stress-induced fear
Prior stress exposure heightens fear learning during Pavlovian fear conditioning. Stress-related increases in ghrelin circulation were shown to be necessary and sufficient for stress to increase fear learning. Ghrelin was found to be upregulated by stress even in the absence of adrenal hormones. Blocking the ghrelin receptor during stress abolished stress-related enhancement of fear memory without blunting other markers of stress. These results suggest that ghrelin is a novel branch of the stress response.[69] Human studies are needed to translate the use of anti-ghrelin treatments to prevent stress-induced psychiatric disorders.
Substantia nigra function
Ghrelin, through its receptor increases the concentration of dopamine in the substantia nigra.[70]
Ghrelin has inhibitory effects on gonadotropin-releasing hormone (GnRH) secretion. It may cause decreased fertility.[71]
Fetus and neonate
Ghrelin is produced early by the fetal lung and promotes lung growth.[72]
Cord blood levels of active and total ghrelin show a correlation between ghrelin levels and birth weight.[50]
Anorexia and obesity
Ghrelin levels in the plasma of obese individuals are lower than those in leaner individuals,[73] suggesting that ghrelin does not contribute to obesity, except in the cases of Prader-Willi syndrome-induced obesity, where high ghrelin levels are correlated with increased food intake.[74][75] However, it is also found that consumption of food for pleasure increased peripheral levels of both ghrelin and the endocannabinoid 2-arachidonoyl-glycerol (2-AG) in healthy humans, and this hedonic eating influences food intake and, ultimately, body mass.[76]
Those with anorexia nervosa have high plasma levels of ghrelin[77] compared to both the constitutionally thin and normal-weight controls.[78][79]
The level of ghrelin increases during the time of day from midnight to dawn in thinner people, which suggests there is a flaw in the circadian rhythm of obese individuals.[80]
Ghrelin levels reflect release in a circadian rhythm, which can be interrupted by exposure to light at night.[81]
Short sleep duration may also lead to obesity, through an increase of appetite via hormonal changes.[82]
Lack of sleep increases ghrelin and decreases leptin, both of which result in increased hunger and obesity.
Ghrelin levels are high in patients with cancer-induced cachexia.[83]
Gastric bypass surgery not only reduces the gut's capacity for food but also dramatically lowers ghrelin levels compared to both lean controls and those that lost weight through dieting alone.[84] However, studies are conflicting as to whether or not ghrelin levels return to nearly normal with gastric bypass patients in the long term after weight loss has stabilized.[85] Bariatric surgeries involving vertical-sleeve gastrectomy reduce plasma ghrelin levels by about 60% in the long term.[86]
Ghrelin plasma concentration increases with age and this may contribute to the tendency for weight gain as people age.[87][88]
Future clinical uses
Synthetic ghrelin administration for cachexia of any cause[89] and for hemodialysis patients[90] is being investigated.
Ghrelin suppresses seizures in animal models and is being investigated.[91]
Ghrelin is a gastric pro-kinetic and may be useful in the treatment of gastroparesis.[92]
Hypothalamic–pituitary–somatic axis
List of growth hormone secretagogues
^a It is important to note that the full mechanism of ghrelin secretion and reduction has not been fully realized, e.g. "this finding appears to discount gastric distention as a mechanism for ghrelin reduction".[93]
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↑ Egecioglu E, Jerlhag E, Salomé N, Skibicka KP, Haage D, Bohlooly-Y M, Andersson D, Bjursell M, Perrissoud D, Engel JA, Dickson SL (July 2010). "Ghrelin increases intake of rewarding food in rodents". Addiction Biology. 15 (3): 304–11. doi:10.1111/j.1369-1600.2010.00216.x. PMC 2901520. PMID 20477752.
↑ Skibicka KP, Hansson C, Egecioglu E, Dickson SL (January 2012). "Role of ghrelin in food reward: impact of ghrelin on sucrose self-administration and mesolimbic dopamine and acetylcholine receptor gene expression". Addiction Biology. 17 (1): 95–107. doi:10.1111/j.1369-1600.2010.00294.x. PMC 3298643. PMID 21309956.
↑ 46.0 46.1 Tolle V, Bassant MH, Zizzari P, Poindessous-Jazat F, Tomasetto C, Epelbaum J, Bluet-Pajot MT (2002). "Ultradian rhythmicity of ghrelin secretion in relation with GH, feeding behavior, and sleep-wake patterns in rats". Endocrinology. 143 (4): 1353–61. doi:10.1210/endo.143.4.8712. PMID 11897692.
↑ Cummings DE, Frayo RS, Marmonier C, Aubert R, Chapelot D (August 2004). "Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues". American Journal of Physiology. Endocrinology and Metabolism. 287 (2): E297–304. doi:10.1152/ajpendo.00582.2003. PMID 15039149.
↑ Wren AM, Small CJ, Ward HL, Murphy KG, Dakin CL, Taheri S, Kennedy AR, Roberts GH, Morgan DG, Ghatei MA, Bloom SR (November 2000). "The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion". Endocrinology. 141 (11): 4325–28. doi:10.1210/endo.141.11.7873. PMID 11089570.
↑ Faulconbridge LF, Cummings DE, Kaplan JM, Grill HJ (September 2003). "Hyperphagic effects of brainstem ghrelin administration". Diabetes. 52 (9): 2260–65. doi:10.2337/diabetes.52.9.2260. PMID 12941764.
↑ 50.0 50.1 Yokota I, Kitamura S, Hosoda H, Kotani Y, Kangawa K (April 2005). "Concentration of the n-octanoylated active form of ghrelin in fetal and neonatal circulation". Endocrine Journal. 52 (2): 271–76. doi:10.1507/endocrj.52.271. PMID 15863960.
↑ Yin Y, Li Y, Zhang W (2014). "The growth hormone secretagogue receptor: its intracellular signaling and regulation". International Journal of Molecular Sciences. 15 (3): 4837–55. doi:10.3390/ijms15034837. PMC 3975427. PMID 24651458.
↑ Waseem T, Duxbury M, Ito H, Rocha F, Lautz D, Whang E, Ashley SW, Robinson MK (September 2004). "Ghrelin ameliorates TNF-a induced anti-proliferative and pro-apoptotic effects and promotes intestinal epithelial restitution". Journal of the American College of Surgeons. 199 (3 Supplement): 16. doi:10.1016/j.jamcollsurg.2004.05.018.
↑ Waseem T, Duxbury M, Ito H, Ashley SW, Robinson MK (March 2008). "Exogenous ghrelin modulates release of pro-inflammatory and anti-inflammatory cytokines in LPS-stimulated macrophages through distinct signaling pathways". Surgery. 143 (3): 334–42. doi:10.1016/j.surg.2007.09.039. PMC 2278045. PMID 18291254.
↑ 54.0 54.1 Gonzalez-Rey E, Chorny A, Delgado M (May 2006). "Therapeutic action of ghrelin in a mouse model of colitis". Gastroenterology. 130 (6): 1707–20. doi:10.1053/j.gastro.2006.01.041. PMID 16697735.
↑ 55.0 55.1 Wu R, Dong W, Ji Y, Zhou M, Marini CP, Ravikumar TS, Wang P (2008). "Orexigenic hormone ghrelin attenuates local and remote organ injury after intestinal ischemia-reperfusion". PLOS One. 3 (4): e2026. Bibcode:2008PLoSO...3.2026W. doi:10.1371/journal.pone.0002026. PMC 2295264. PMID 18431503.
↑ Işeri SO, Sener G, Yüksel M, Contuk G, Cetinel S, Gedik N, Yegen BC (December 2005). "Ghrelin against alendronate-induced gastric damage in rats". Journal of Endocrinology. 187 (3): 399–406. doi:10.1677/joe.1.06432. PMID 16423819.
↑ Waseem T (March 2010). "Commentary: Ghrelin's role in gastrointestinal tract cancer". Surgical Oncology. 19 (1): e1. doi:10.1016/j.suronc.2009.02.014. PMID 19324542.
↑ Waseem T, Ahmad F, Azam M, Qureshi MA (August 2008). "Role of ghrelin axis in colorectal cancer: a novel association". Peptides. 29 (8): 1369–76. doi:10.1016/j.peptides.2008.03.020. PMID 18471933.
↑ Duxbury MS, Waseem T, Ito H, Robinson MK, Zinner MJ, Ashley SW, Whang EE (September 2003). "Ghrelin promotes pancreatic adenocarcinoma cellular proliferation and invasiveness". Biochemical and Biophysical Research Communications. 309 (2): 464–68. doi:10.1016/j.bbrc.2003.08.024. PMID 12951072.
↑ Michael R. DiGruccio; Alex M. Mawla; Cynthia J. Donaldson; Glyn M. Noguchi; Joan Vaughan; Christopher Cowing-Zitron; Talitha van der Meulen; Mark O. Huising (2016-05-02). "Comprehensive alpha, beta and delta cell transcriptomes reveal that ghrelin selectively activates delta cells and promotes somatostatin release from pancreatic islets". Molecular Metabolism. 5 (7): 449–58. doi:10.1016/j.molmet.2016.04.007. PMC 4921781. PMID 27408771. Retrieved 2016-05-30.
↑ Heppner KM, Tong J (July 2014). "Mechanisms in endocrinology: regulation of glucose metabolism by the ghrelin system: multiple players and multiple actions". European Journal of Endocrinology. 171 (1): R21–32. doi:10.1530/EJE-14-0183. PMID 24714083.
↑ 62.0 62.1 Diano S, Farr SA, Benoit SC, McNay EC, da Silva I, Horvath B, Gaskin FS, Nonaka N, Jaeger LB, Banks WA, Morley JE, Pinto S, Sherwin RS, Xu L, Yamada KA, Sleeman MW, Tschöp MH, Horvath TL (March 2006). "Ghrelin controls hippocampal spine synapse density and memory performance". Nature Neuroscience. 9 (3): 381–88. doi:10.1038/nn1656. PMID 16491079. Lay summary – Science Blog.
↑ Atcha Z, Chen WS, Ong AB, Wong FK, Neo A, Browne ER, Witherington J, Pemberton DJ (October 2009). "Cognitive enhancing effects of ghrelin receptor agonists". Psychopharmacology. 206 (3): 415–27. doi:10.1007/s00213-009-1620-6. PMID 19652956.
↑ Cahill SP, Hatchard T, Abizaid A, Holahan MR (2014). "An examination of early neural and cognitive alterations in hippocampal-spatial function of ghrelin receptor-deficient rats". Behavioural Brain Research. 264: 105–15. doi:10.1016/j.bbr.2014.02.004. PMID 24525421.
↑ Stengel A, Taché Y (2012). "Ghrelin – a pleiotropic hormone secreted from endocrine x/a-like cells of the stomach". Frontiers in Neuroscience. 6: 24. doi:10.3389/fnins.2012.00024. PMC 3280431. PMID 22355282.
↑ 66.0 66.1 Spencer SJ, Xu L, Clarke MA, Lemus M, Reichenbach A, Geenen B, Kozicz T, Andrews ZB (September 2012). "Ghrelin regulates the hypothalamic-pituitary-adrenal axis and restricts anxiety after acute stress". Biological Psychiatry. 72 (6): 457–65. doi:10.1016/j.biopsych.2012.03.010. PMID 22521145.
↑ Lutter M, Sakata I, Osborne-Lawrence S, Rovinsky SA, Anderson JG, Jung S, Birnbaum S, Yanagisawa M, Elmquist JK, Nestler EJ, Zigman JM (July 2008). "The orexigenic hormone ghrelin defends against depressive symptoms of chronic stress". Nature Neuroscience. 11 (7): 752–53. doi:10.1038/nn.2139. PMC 2765052. PMID 18552842.
↑ Taheri S, Lin L, Austin D, Young T, Mignot E (December 2004). "Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index". PLOS Medicine. 1 (3): e62. doi:10.1371/journal.pmed.0010062. PMC 535701. PMID 15602591.
↑ Meyer RM, Burgos-Robles A, Liu E, Correia SS, Goosens KA (December 2014). "A ghrelin-growth hormone axis drives stress-induced vulnerability to enhanced fear". Molecular Psychiatry. 19 (12): 1284–94. doi:10.1038/mp.2013.135. PMC 3988273. PMID 24126924. Lay summary – Massachusetts Institute of Technology News.
↑ Andrews ZB, Erion D, Beiler R, Liu ZW, Abizaid A, Zigman J, Elsworth JD, Savitt JM, DiMarchi R, Tschoep M, Roth RH, Gao XB, Horvath TL (November 2009). "Ghrelin promotes and protects nigrostriatal dopamine function via a UCP2-dependent mitochondrial mechanism". The Journal of Neuroscience. 29 (45): 14057–65. doi:10.1523/JNEUROSCI.3890-09.2009. PMC 2845822. PMID 19906954.
↑ Comninos AN, Jayasena CN, Dhillo WS (2014). "The relationship between gut and adipose hormones, and reproduction". Human Reproduction Update. 20 (2): 153–74. doi:10.1093/humupd/dmt033. PMID 24173881.
↑ Santos M, Bastos P, Gonzaga S, Roriz JM, Baptista MJ, Nogueira-Silva C, Melo-Rocha G, Henriques-Coelho T, Roncon-Albuquerque R, Leite-Moreira AF, De Krijger RR, Tibboel D, Rottier R, Correia-Pinto J (April 2006). "Ghrelin expression in human and rat fetal lungs and the effect of ghrelin administration in nitrofen-induced congenital diaphragmatic hernia". Pediatric Research. 59 (4 Pt 1): 531–37. doi:10.1203/01.pdr.0000202748.66359.a9. PMID 16549524.
↑ Shiiya, T; Nakazato, M; Mizuta, M; Date, Y; Mondal, MS; Tanaka, M; Nozoe, S; Hosoda, H; Kangawa, K; Matsukura, S (January 2002). "Plasma ghrelin levels in lean and obese humans and the effect of glucose on ghrelin secretion". The Journal of Clinical Endocrinology and Metabolism. 87 (1): 240–44. doi:10.1210/jcem.87.1.8129. PMID 11788653.
↑ Goldstone AP, Thomas EL, Brynes AE, Castroman G, Edwards R, Ghatei MA, Frost G, Holland AJ, Grossman AB, Korbonits M, Bloom SR, Bell JD (April 2004). "Elevated fasting plasma ghrelin in prader-willi syndrome adults is not solely explained by their reduced visceral adiposity and insulin resistance". The Journal of Clinical Endocrinology and Metabolism. 89 (4): 1718–26. doi:10.1210/jc.2003-031118. PMID 15070936.
↑ DelParigi A, Tschöp M, Heiman ML, Salbe AD, Vozarova B, Sell SM, Bunt JC, Tataranni PA (December 2002). "High circulating ghrelin: a potential cause for hyperphagia and obesity in prader-willi syndrome". The Journal of Clinical Endocrinology and Metabolism. 87 (12): 5461–64. doi:10.1210/jc.2002-020871. PMID 12466337.
↑ Monteleone, Palmiero; Piscitelli, Fabiana; Scognamiglio, Pasquale; Monteleone, Alessio Maria; Canestrelli, Benedetta; Di Marzo, Vincenzo; Maj, Mario (2012-06-01). "Hedonic eating is associated with increased peripheral levels of ghrelin and the endocannabinoid 2-arachidonoyl-glycerol in healthy humans: a pilot study". The Journal of Clinical Endocrinology and Metabolism. 97 (6): E917–24. doi:10.1210/jc.2011-3018. ISSN 1945-7197. PMID 22442280.
↑ Misra M, Klibanski A (July 2014). "Endocrine consequences of anorexia nervosa". The Lancet Diabetes & Endocrinology. 2 (7): 581–92. doi:10.1016/S2213-8587(13)70180-3. PMC 4133106. PMID 24731664.
↑ Tolle V, Kadem M, Bluet-Pajot MT, Frere D, Foulon C, Bossu C, Dardennes R, Mounier C, Zizzari P, Lang F, Epelbaum J, Estour B (2003). "Balance in ghrelin and leptin plasma levels in anorexia nervosa patients and constitutionally thin women". The Journal of Clinical Endocrinology and Metabolism. 88 (1): 109–16. doi:10.1210/jc.2002-020645. PMID 12519838.
↑ Germain N, Galusca B, Le Roux CW, Bossu C, Ghatei MA, Lang F, Bloom SR, Estour B (April 2007). "Constitutional thinness and lean anorexia nervosa display opposite concentrations of peptide YY, glucagon-like peptide 1, ghrelin, and leptin". The American Journal of Clinical Nutrition. 85 (4): 967–71. doi:10.1093/ajcn/85.4.967. PMID 17413094.
↑ Yildiz BO, Suchard MA, Wong ML, McCann SM, Licinio J (July 2004). "Alterations in the dynamics of circulating ghrelin, adiponectin, and leptin in human obesity". Proceedings of the National Academy of Sciences of the United States of America. 101 (28): 10434–39. Bibcode:2004PNAS..10110434Y. doi:10.1073/pnas.0403465101. PMC 478601. PMID 15231997.
↑ Fonken LK, Nelson RJ (April 2014). "The effects of light at night on circadian clocks and metabolism". Endocrine Reviews. 35 (4): 648–70. doi:10.1210/er.2013-1051. PMID 24673196.
↑ Cappuccio FP, Taggart FM, Kandala NB, Currie A, Peile E, Stranges S, Miller MA (May 2008). "Meta-analysis of short sleep duration and obesity in children and adults". Sleep. 31 (5): 619–26. doi:10.1093/sleep/31.5.619. PMC 2398753. PMID 18517032.
↑ Garcia JM, Garcia-Touza M, Hijazi RA, Taffet G, Epner D, Mann D, Smith RG, Cunningham GR, Marcelli M (May 2005). "Active ghrelin levels and active to total ghrelin ratio in cancer-induced cachexia". The Journal of Clinical Endocrinology and Metabolism. 90 (5): 2920–26. doi:10.1210/jc.2004-1788. PMID 15713718.
↑ Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, Purnell JQ (May 2002). "Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery". The New England Journal of Medicine. 346 (21): 1623–30. doi:10.1056/NEJMoa012908. PMID 12023994.
↑ Cummings DE, Shannon MH (July 2003). "Ghrelin and gastric bypass: is there a hormonal contribution to surgical weight loss?". The Journal of Clinical Endocrinology and Metabolism. 88 (7): 2999–3002. doi:10.1210/jc.2003-030705. PMID 12843132.
↑ Bohdjalian A, Langer FB, Shakeri-Leidenmühler S, Gfrerer L, Ludvik B, Zacherl J, Prager G (May 2010). "Sleeve gastrectomy as sole and definitive bariatric procedure: 5-year results for weight loss and ghrelin". Obesity Surgery. 20 (5): 535–40. doi:10.1007/s11695-009-0066-6. PMID 20094819.
↑ Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse BE, Weigle DS (August 2001). "A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans". Diabetes. 50 (8): 1714–19. doi:10.2337/diabetes.50.8.1714. PMID 11473029.
↑ Karasu SR, Karasu TB (2010). The gravity of weight: a clinical guide to weight loss and maintenance (1st ed.). Washington, DC: American Psychiatric Publishing. p. 162. ISBN 978-1585623600.
↑ Berardi E, Annibali D, Cassano M, Crippa S, Sampaolesi M (2014). "Molecular and cell-based therapies for muscle degenerations: a road under construction". Frontiers in Physiology. 5: 119. doi:10.3389/fphys.2014.00119. PMC 3986550. PMID 24782779.
↑ Ruperto M, Sánchez-Muniz FJ, Barril G (2014). "A clinical approach to the nutritional care process in protein-energy wasting hemodialysis patients". Nutrición Hospitalaria. 29 (4): 735–50. doi:10.3305/nh.2014.29.4.7222. PMID 24679014.
↑ Clynen E, Swijsen A, Raijmakers M, Hoogland G, Rigo JM (October 2014). "Neuropeptides as targets for the development of anticonvulsant drugs". Molecular Neurobiology. 50 (2): 626–46. doi:10.1007/s12035-014-8669-x. PMC 4182642. PMID 24705860.
↑ Hasler WL (June 2014). "Emerging drugs for the treatment of gastroparesis". Expert Opinion on Emerging Drugs. 19 (2): 261–79. doi:10.1517/14728214.2014.899353. PMID 24669936.
↑ Williams DL, Cummings DE, Grill HJ, Kaplan JM (2003). "Meal-Related Ghrelin Suppression Requires Postgastric Feedback". Endocrinology. 144 (7): 2765–67. doi:10.1210/en.2003-0381. PMID 12810528.
File:Wiktionary-logo-en-v2.svg Look up ghrelin in Wiktionary, the free dictionary.
Hypothalamic-
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neuropeptides
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Cocaine- and amphetamine-regulated transcript
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GH/IGF-1 axis signaling modulators
(somatotropin)
Agonists: Albusomatropin
Bovine somatotropin
Efpegsomatropin
Eftansomatropin alfa
Human placental lactogen
Placental growth hormone (growth hormone variant)
Somagrebove
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Somatrem
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Somatrogon (MOD-4023; hGH-CTP)
Somavaratan
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Antagonists: G120K-hGH
Pegvisomant
Antisense oligonucleotides: Atesidorsen
Binding proteins: GHBP
GHIH
(somatostatin)
Agonists: BIM-23052
Cortistatin-14
Depreotide
Edotreotide
Ilatreotide
L-803,087
Lanreotide
NNC 26-9100
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Octreotide
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Seglitide
Somatostatin (1-28)
SRIF-14
TT-232
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Antagonists: BIM-23056
Cyclosomatostatin
CYN-154806
Satoreotide
(somatocrinin)
Agonists: Peptide: ALRN-5281
CJC-1295
Dumorelin
Modified GRF (1-29)
Rismorelin
Somatorelin
Antagonists: MZ-5-156
(ghrelin)
Agonists: Peptide: Alexamorelin
EP-51216
Examorelin (hexarelin)
Lenomorelin
Livoletide
LY-444711
Pralmorelin (GHRP-2)
Relamorelin
Tabimorelin
Ulimorelin; Non-peptide: Adenosine
Anamorelin
Capromorelin
CP-464709
Ibutamoren (MK-677)
Macimorelin
SM-130686; Unsorted: LY-426410
Antagonists: A-778193
Cortistatin-8
(D-Lys³)-GHRP-6
JMV2959
YIL-781
(somatomedin)
See here instead.
See also: Receptor/signaling modulators • Signaling peptide/protein receptor modulators
Retrieved from "https://www.wikidoc.org/index.php?title=Ghrelin&oldid=1532456"
Genes on human chromosome
Appetite stimulants
Ghrelin receptor agonists
Growth hormone secretagogues
Hormones of the somatotropic axis
Peptide hormones
World Anti-Doping Agency prohibited substances
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