WordNet
- a gastrointestinal hormone produced by epithelial cells lining the fundus of the stomach; appears to be a stimulant for appetite and feeding, but is also a strong stimulant of growth hormone secretion from the anterior pituitary
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/06/08 22:59:26」(JST)
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| Aliases | GHRL, MTLRP, ghrelin/obestatin prepropeptide | ||||||||||||||||
| External IDs | MGI: 1930008 HomoloGene: 9487 GeneCards: 51738 | ||||||||||||||||
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| Location (UCSC) | Chr 3: 10.29 – 10.29 Mb | Chr 6: 113.72 – 113.72 Mb | |||||||||||||||
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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] which 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 (GHSR), 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]
Contents
- 1 History and name
- 2 Gene, transcription products, and structure
- 3 Ghrelin cells
- 3.1 Alternate names
- 3.2 Location
- 3.3 Features
- 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 Immune system
- 9 Anorexia and obesity
- 10 Disease management
- 10.1 Gastric bypass surgery
- 10.2 Medical management of obesity
- 11 Aging
- 12 Future clinical uses
- 13 Notes
- 14 References
- 15 Further reading
History and name
Ghrelin was discovered after the ghrelin receptor (called growth hormone secretagogue type 1A receptor or GHSR) 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
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 GHSR 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
Alternate names
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]
Location
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]
Features
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 also improves endothelial function and inhibits proatherogenic changes in cell cultures. It activates the endothelial isoform of nitric oxide synthase in a pathway that depends on various kinases including Akt.[46]
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.[47][48] Injections of ghrelin in both humans and rats have been shown to increase food intake in a dose-dependent manner.[49] So the more ghrelin that is injected the more food that is consumed. However, ghrelin does not increase meal size, only meal number.[50] 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] When a person loses weight their ghrelin levels increase, which causes increased food consumption and weight gain. On the other hand, when a person gains weight, ghrelin levels drop, leading to a decrease in food consumption and weight loss. This suggests that ghrelin acts as a body weight regulator, continuously keeping one's body weight and energy stores in check.
Blood levels
Blood levels are in the pmol/l range. Both active and total ghrelin can be measured.[51] Circulating ghrelin concentrations rise before eating and fall afterward,[47] more strongly in response to protein and carbohydrate than to lipids.[21]
Ghrelin receptor
The ghrelin receptor GHSR1a (a splice-variant of the growth hormone secretagogue receptor, with the GHSR1b 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.[52] 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
Gastrointestinal tract
Ghrelin promotes intestinal cell proliferation and inhibits apoptosis during inflammatory states and oxidative stress.[53][54] 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.[55][56] Animal models of colitis, ischemia reperfusion, and sepsis-related gut dysfunction have been shown to benefit from therapeutic doses of ghrelin.[55][56] It has also been shown to have regenerative capacity and is beneficial in mucosal injury to the stomach.[57]
Ghrelin promotes gastrointestinal and pancreatic malignancy.[58][59][60]
Pancreas
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. [61]
Glucose metabolism
The entire ghrelin system (dAG, AG, GHSR and GOAT) has a gluco-regulatory action.[62]
Nervous system
Learning and memory
The hippocampus plays a significant role in neurotrophy: the cognitive adaptation to changing environments and the process of learning[63][64] 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.[65] 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.[63] In rodents, X/A-like cells produce ghrelin.[66]
Depression
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.[67] In normal mice, ghrelin can stimulate the hypothalamic-pituitary-adrenal axis, from the anterior pituitary.[67]
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.[68] 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.[69]
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.[70] 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.[71]
Reproductive system
Ghrelin has inhibitory effects on gonadotropin-releasing hormone (GnRH) secretion. It may cause decreased fertility.[72]
Fetus and neonate
- Ghrelin is produced early by the fetal lung and promotes lung growth.[73]
- Cord blood levels of active and total ghrelin show a correlation between ghrelin levels and birth weight.[51]
Immune system
Ghrelin gene products have several actions on acute and chronic inflammation and autoimmunity, with promising therapeutic applications.[74]
Anorexia and obesity
- Ghrelin levels in the plasma of obese individuals are lower than those in leaner individuals,[75] 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.[76][77]
- Those with anorexia nervosa have high plasma levels of ghrelin[78] compared to both the constitutionally thin and normal-weight controls.[79][80]
- 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.[81]
- Ghrelin levels reflect release in a circadian rhythm which can be interrupted by exposure to light at night.[82]
- Short sleep duration may also lead to obesity, through an increase of appetite via hormonal changes.[83]
- Lack of sleep increases ghrelin, and decreases leptin, both effects producing increased hunger and obesity.
- Ghrelin levels are high in patients with cancer-induced cachexia.[84]
Disease management
Gastric bypass surgery
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.[75] 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]
Medical management of obesity
Ghrelin is not FDA approved for any indication.
In rodents and pigs, an anti-obesity vaccine has been developed: it blocks the ghrelin receptor.[87][88]
Aging
Ghrelin plasma concentration increases with age and this may contribute to the tendency for weight gain as people age.[89][90]
Future clinical uses
- Synthetic ghrelin administration for cachexia of any cause[91] and for hemodialysis patients[92] is being investigated.
- Ghrelin suppresses seizures in animal models and is being investigated.[93]
- Ghrelin is a gastric pro-kinetic and may be useful in the treatment of gastroparesis.[94]
Notes
- ^a Caution should be taken, it is not unanimous this sentence, e.g. "this finding appears to discount gastric distention as a mechanism for ghrelin reduction".[95]
References
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Whereas ghrelin emerged as a stomach-derived hormone involved in energy balance, hunger and meal initiation via hypothalamic circuits, it now seems clear that it also has a role in motivated reward-driven behaviours via activation of the so-called "cholinergic-dopaminergic reward link". This reward link comprises a dopamine projection from the ventral tegmental area (VTA) to the nucleus accumbens together with a cholinergic input, arising primarily from the laterodorsal tegmental area. Ghrelin administration into the VTA or LDTg activates the "cholinergic-dopaminergic" reward link, suggesting that ghrelin may increase the incentive value of motivated behaviours such as reward-seeking behaviour ("wanting" or "incentive motivation").
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The best described site of action of ghrelin is the VMH and arcuate nucleus, but ghrelin receptors are also expressed in the brain’s reward pathways (eg, VTA dopamine neurons) and may stimulate feeding through this action as well. ... It is very interesting then, as mentioned above, that orexin, leptin, and ghrelin receptors are expressed in the VTA, and MC4 and MCH receptors are enriched in the nucleus accumbens. There is increasing evidence that some of the actions of these feeding peptides are mediated at the level of the VTA-NAc circuit: recent studies, for example, have shown that injection of leptin into the VTA suppresses feeding behavior, while RNAi (RNA interference; Chapter 4) mediated-knockdown of leptin receptors in the VTA increases food intake, sensitivity to highly palatable foods, and locomotor activity.
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- ^ 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. doi:10.1016/j.molmet.2016.04.007. Retrieved 2016-05-30. CS1 maint: Multiple names: authors list (link)
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- ^ a b 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.
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- ^ 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.
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- ^ Prodam F, Filigheddu N (October 2014). "Ghrelin gene products in acute and chronic inflammation". Archivum Immunologiae et Therapiae Experimentalis 62 (5): 369–84. doi:10.1007/s00005-014-0287-9. PMID 24728531.
- ^ a b 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.
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Further reading
- 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.
- Dickson SL (January 2002). "Ghrelin: a newly discovered hormone". Journal of Neuroendocrinology 14 (1): 83–4. PMID 11903816.
- Bown R (3 September 2006). "Ghrelin". Pathophysiology of the Endocrine System. Colorado State University. Retrieved 18 September 2008.
- Burstain T (1 January 2005). "Balancing Your Hunger Hormones". Web site reviewing role of ghrelin and leptin in obesity. Infinity Medical Systems, Inc. Retrieved 18 September 2008.
- Shea C (10 December 2006). "Empty-Stomach Intelligence". New York Times. Retrieved 18 September 2008.
- Raloff J (April 2005). "Still Hungry? Fattening revelations—and new mysteries—about the hunger hormone". Science News (ScienceNews.org) 167 (14): 216–220. doi:10.2307/4016366. JSTOR 4016366.
- Nixon R (14 July 2008). "Feeling hungry can make you happy". Mental health (MSNBC.com). Retrieved 18 September 2008.
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UpToDate Contents
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- 1. グレリン ghrelin
- 2. 肥満への遺伝的影響と病態生理 genetic contribution and pathophysiology of obesity
- 3. 癌における食欲不振および悪液質の薬理学的マネージメント pharmacologic management of cancer anorexia cachexia
- 4. 成長ホルモンの生理学 physiology of growth hormone
- 5. プラダーウィリ症候群の臨床的特徴、診断、および治療 clinical features diagnosis and treatment of prader willi syndrome
English Journal
- Effects of weight loss diet therapy on anthropometric measurements and biochemical variables in schizophrenic patients.
- Urhan M1, Ergün C, Aksoy M, Ayer A.
- Nordic journal of psychiatry.Nord J Psychiatry.2015 Jul;69(5):323-30. doi: 10.3109/08039488.2014.981288. Epub 2015 May 18.
- BACKGROUND: Prevalence of obesity in schizophrenic patients is two to three times higher than in the general population and unhealthy dietary patterns, a sedentary lifestyle and antipsychotic medication use may contribute to the higher levels of obesity among schizophrenic patients.AIMS: We evaluate
- PMID 25981354
- Ghrelin-reactive immunoglobulins and anxiety, depression and stress-induced cortisol response in adolescents. The TRAILS study.
- François M1, Schaefer JM2, Bole-Feysot C1, Déchelotte P1, Verhulst FC2, Fetissov SO3.
- Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2015 Jun 3;59:1-7. doi: 10.1016/j.pnpbp.2014.12.011. Epub 2015 Jan 3.
- BACKGROUND: Ghrelin, a hunger hormone, has been implicated in the regulation of stress-response, anxiety and depression. Ghrelin-reactive immunoglobulins (Ig) were recently identified in healthy and obese humans showing abilities to increase ghrelin's stability and orexigenic effects. Here we studie
- PMID 25562566
- Appetite and gut hormone responses to moderate-intensity continuous exercise versus high-intensity interval exercise, in normoxic and hypoxic conditions.
- Bailey DP1, Smith LR2, Chrismas BC2, Taylor L2, Stensel DJ3, Deighton K3, Douglas JA3, Kerr CJ4.
- Appetite.Appetite.2015 Jun;89:237-45. doi: 10.1016/j.appet.2015.02.019. Epub 2015 Feb 17.
- This study investigated the effects of continuous moderate-intensity exercise (MIE) and high-intensity interval exercise (HIIE) in combination with short exposure to hypoxia on appetite and plasma concentrations of acylated ghrelin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). Twelve healt
- PMID 25700630
- Fed and fasted chicks from lines divergently selected for low or high body weight have differential hypothalamic appetite-associated factor mRNA expression profiles.
- Yi J1, Gilbert ER1, Siegel PB1, Cline MA2.
- Behavioural brain research.Behav Brain Res.2015 Jun 1;286:58-63. doi: 10.1016/j.bbr.2015.02.008. Epub 2015 Feb 10.
- We have demonstrated that chicken lines which have undergone intense divergent selection for either low (LWS) or high (HWS) body weight (anorexic and obese containing, respectively) have differential food intake threshold responses to a range of intracerebroventricular injected neurotransmitters. Th
- PMID 25677648
Japanese Journal
- Ghrelin-induced hypophagia is mediated by the β₂ adrenergic receptor in chicken
- Zendehdel Morteza,Hassanpour Shahin
- The journal of physiological sciences 64(5), 383-391, 2014-09
- NAID 40020178499
- グレリン,グルカゴン様ペプチド1と迷走神経 (第5土曜特集 肥満の医学 : 臨床と研究の最先端) -- (中枢と末梢の臓器間ネットワーク)
- 十枝内 厚次,ワイズ T. M. ザベット,中里 雅光
- 医学のあゆみ 250(9), 773-777, 2014-08-30
- NAID 40020171511
- 迷走神経を介した消化管ペプチドによる摂食調節
- 十枝内 厚次,Waise TM Zaved,中里 雅光
- 内分泌・糖尿病・代謝内科 39(1), 62-68, 2014-07
- NAID 40020175887
- 神経内分泌学の歴史と現状 (特集 拡がりゆく神経内分泌学の現状と展望)
- 山口 秀樹,中里 雅光,寒川 賢治
- 内分泌・糖尿病・代謝内科 39(1), 2-9, 2014-07
- NAID 40020175681
Related Links
- Ghrelin
- ホーム 新製品・新技術情報 Ghrelin Ghrelin [新しいタイプの内因性成長ホルモン分泌促進ペプチド見つかる！] 成長ホルモン放出作用を持つ内因性物質にはアミノ酸44残基からなる growth-hormone-releasing factor (GRF) があり、視床下部から ...
- 今回発売させて頂くキットは、Active Ghrelin ELISA Kit/Desacyl-ghrelin ELISA Kitです。 ともに2種類のモノクローナル抗体を用いる酵素免疫測定法（ELISA法）で、高感度で特異性が高いという特徴を持っています。 これまでグレリンに関して ...
Related Pictures
★リンクテーブル★
| リンク元 | 「下垂体前葉ホルモン」「グレリン」 |
| 拡張検索 | 「ghrelin receptor」 |
「下垂体前葉ホルモン」
分泌されるホルモン
- 単純ペプチドホルモン
- 糖タンパク質ホルモン
GOO. chapter 55
| 名称 | 構造 | 分泌細胞 | 下垂体前葉細胞 全細胞に対する 産生細胞の割合 |
染色性 | サブユニット | 残基数 (aa.) |
分子量 (kDa) |
その他 | ||
| 成長ホルモン | GH | ペプチド | somatotroph | 40-50% | 好酸性 | 1 | 191 | 22 | ||
| プロラクチン | PRL | mammotroph | 10-25% | 好酸性 | 1 | 199 | 23 | |||
| 副腎皮質刺激ホルモン | ACTH | corticotroph | 0.1 | 好塩基性 | 嫌色素性 | 1 | 39 | 4.5 | POMC由来 | |
| 甲状腺刺激ホルモン | TSH | 糖タンパク | thyrotroph | 0.05 | 好塩基性 | 2 | α: 92, β:118 | 28 | αサブユニットは共通 | |
| 卵胞刺激ホルモン | FSH | gonadotroph | 10-15% | 好塩基性 | 2 | α: 92, β:111 | 32.6 | |||
| 黄体形成ホルモン | LH | 好塩基性 | 2 | α: 92, β:121 | 29.4 | |||||
HIM.2196
| Table 333-1 Anterior Pituitary Hormone Expression and Regulation | |||||
| Cell | corticotrope | somatotrope | lactotrope | thyrotrope | gonadotrope |
| Tissue-specific transcription factor | T-Pit | Prop-1, Pit-1 | Prop-1, Pit-1 | Prop-1, Pit-1, TEF | SF-1, DAX-1 |
| Fetal appearance | 6 weeks | 8 weeks | 12 weeks | 12 weeks | 12 weeks |
| Hormone | POMC | GH | PRL | TSH | FSH LH |
| Chromosomal locus | 2p | 17q | 6 | －6q; －1p | －11p; －19q |
| Protein | ポリペプチド | 糖タンパク | |||
| Amino acids | 266 (ACTH 1–39) | 191 | 199 | 211 | 210 204 |
| Stimulators | CRH, AVP, gp-130 cytokines | GHRH, ghrelin, bromocriptine(1) | estrogen, TRH, VIP | TRH | GnRH, activins, estrogen |
| Inhibitors | glucocorticoids | somatostatin, IGF-I | dopamine | T3, T4, dopamine, somatostatin, glucocorticoids | sex steroids, inhibin |
| Target gland | adrenal | liver, other tissues | breast, other tissues | thyroid | ovary, testis |
| Trophic effect | steroid production | IGF-I production, growth induction, insulin antagonism | milk production | T4 synthesis and secretion | sex steroid production, follicle growth, germ cell maturation |
- (1):QB.D-253