NPY

• ニューロペプチドY

関

neuropeptide Y

同

neuropeptide Y

WordNet

1. the 14th letter of the Roman alphabet (同)n

PrepTutorEJDIC

1. nitrogenの化学記号

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/12/22 04:40:46」(JST)

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Neuropeptide Y
Structure of Neuropeptide Y. From PDB 1ron.
Available structures PDB Ortholog search: PDBe, RCSB List of PDB id codes 1QFA, 1RON
Identifiers
Symbols	NPY; PYY4
External IDs	OMIM: 162640 MGI: 97374 HomoloGene: 697 GeneCards: NPY Gene
Gene Ontology Molecular function • G-protein coupled receptor binding • G-protein coupled receptor activity • receptor binding • neuropeptide hormone activity • calcium channel regulator activity Cellular component • extracellular region • extracellular space • cell Biological process • calcium ion transport • cellular component movement • G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger • neuropeptide signaling pathway • synaptic transmission • digestion • behavior • feeding behavior • blood circulation • regulation of blood pressure • cell proliferation • adult feeding behavior • central nervous system neuron development • cerebral cortex development • neuron projection development • positive regulation of appetite Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	4852	109648
Ensembl	ENSG00000122585	ENSMUSG00000029819
UniProt	P01303	P57774
RefSeq (mRNA)	NM_000905	NM_023456
RefSeq (protein)	NP_000896	NP_075945
Location (UCSC)	Chr 7: 24.32 – 24.33 Mb	Chr 6: 49.82 – 49.83 Mb
PubMed search	[1]	[2]

Neuropeptide Y

Clinical data
Pregnancy cat.	?
Legal status	?
Identifiers
CAS number	82785-45-3 N
ATC code	?
ChEMBL	CHEMBL267633 N
Chemical data
Formula	C190H287N55O57
Mol. mass	4253.7 g/mol
N (what is this?)  (verify)

Neuropeptide Y (NPY) is a 36-amino acid neuropeptide that acts as a neurotransmitter in the brain and in the autonomic nervous system of humans; slight variations of the peptide are found in many other animals. In the autonomic system it is mainly produced by neurons of the sympathetic nervous system and serves as a strong vasoconstrictor and also causes growth of fat tissue. In the brain it is produced in various locations including the hypothalamus, and is thought to have several functions, including: increasing food intake and storage of energy as fat, reducing anxiety and stress, reducing pain perception, affecting the circadian rhythm, reducing voluntary alcohol intake, lowering blood pressure and controlling epileptic seizures.

Discovery

Following the isolation of neuropeptide-y (NPY) from the porcine hypothalamus in 1982, researchers began to speculate about the involvement of NPY in hypothalamic-mediated functions. In a 1983 study, NPY-ergic axon terminals were located in the paraventricular nucleus (PVN) of the hypothalamus, and the highest levels of NPY immunoreactivity was found within the PVN of the hypothalamus.

Six years later, in 1989, Morris et al. homed in on the location of NPYergic nuclei in the brain. Furthermore, in situ hybridization results from the study showed the highest cellular levels of NPY mRNA in the arcuate nucleus (ARC) of the hypothalamus.

In 1989, Haas & George reported that local injection of NPY into the PVN resulted in an acute release of corticotropin-releasing hormone (CRH) in the rat brain, proving that NPYergic activity directly stimulates the release and synthesis of CRH.

The latter became a hallmark paper in NPY studies. A significant amount of work had already been done in the 1970s on CRH and its involvement in stress and eating disorders such as obesity. These studies, collectively, marked the beginning of the role of NPY in orexigenesis or food intake.

The role of NPY in food intake

Behaviorial assays in orexigenic studies, in which rats are the model organism, have been done collectively with immunoassays and in situ hybridization studies to confirm that elevating NPYergic activity does indeed increase food intake. In these studies, exogenous NPY, an NPY agonist such as dexamethasone or N-acetyl [Leu 28, Leu31] NPY (24-36) are injected into the third ventricle or at the level of the hypothalamus with a cannula.

Furthermore, these studies unanimously demonstrate that the stimulation of NPYergic activity via the administration of certain NPY agonists increases food intake compared to baseline data in rats. The effects of NPYergic activity on food intake is also demonstrated by the blockade of certain NPY receptors (Y1 and Y5 receptors), which, as was expected, inhibited NPYergic activity; thus, decreases food intake. However, a 1999 study by King et al. demonstrated the effects of the activation of the NPY autoreceptor Y2, which has been shown to inhibit the release of NPY and thus acts to regulate food intake upon its activation. In this study a highly selective Y2 antagonist, BIIE0246 was administered locally into the ARC. Radioimmunoassay data, following the injection of BIIE0246, shows a significant increase in NPY release compared to the control group. Though the pharmacological half-life of exogenous NPY, other agonists, and antagonist is still obscure, the effects are not long lasting and the rat body employs an excellent ability to regulate and normalize abnormal NPY levels and therefore food consumption.

The role of NPY in obesity

Dryden et al., conducted a study in 1995 using genetically obese rats to demonstrate the role of NPY in eating disorders such as obesity. The study revealed four underlying factors that contributed to obesity in rats:

• an increase in glucocorticosteroid concentrations in plasma;
• insensitivity or resistance to insulin;
• mutation of leptin receptor; and
• an increase in NPY mRNA and NPY release.

Furthermore, these factors correlate with each other. The sustained high levels of glucocorticosteroids stimulate gluconeogenesis, which subsequently causes an increase of blood glucose that activates the release of insulin to regulate glucose levels by causing its reuptake and storage as glycogen in the tissues in the body. In the case of obesity, which researchers speculate to have a strong genetic and a dietary basis, insulin resistance prevents high blood glucose regulation, resulting in morbid levels of glucose and diabetes mellitus. In addition, high levels of glucocorticosteroids causes an increase of NPY by directly activating type II glucocorticosteroids receptors (which are activated only by relatively high levels of glucocorticosteroids) and, indirectly, by abolishing the negative feedback of corticotropin-releasing factor (CRF) on NPY synthesis and release. Meanwhile, obesity-induced insulin resistance and the mutation of the leptin receptor (ObRb) results in the abolition of inhibition of NPYergic activity and ultimately food intake via other negative feedback mechanisms to regulate them. Obesity in rats was significantly reduced by adrenalectomy or hypophysectomy.

Correlation with stress and diet

Studies of mice and monkeys show that repeated stress — and a high-fat, high-sugar diet — stimulate the release of neuropeptide Y, causing fat to build up in the abdomen. Researchers believe that by manipulating levels of NPY, they could make fat melt from areas where it was not desired and accumulate at sites where it is needed.

Higher levels of NPY may be associated with resilience against and recovery from posttraumatic stress disorder and with dampening the fear response, allowing individuals to perform better under extreme stress.

Alcoholism

Two results suggest that NPY might protect against alcoholism:

• knock-out mice in which a type of NPY receptor has been removed show a higher voluntary intake of alcohol and a higher resistance to alcohol's sedating effects, compared to normal mice;
• the common fruit fly has a neuropeptide that is similar to NPY, known as neuropeptide F. The levels of neuropeptide F are lowered in sexually frustrated male flies, and this causes the flies to increase their voluntary intake of alcohol.

Receptors

Main article: Neuropeptide Y receptor

The receptor protein that NPY operates on is a G protein-coupled receptor in the rhodopsin like 7-transmembrane GPCR family. Five subtypes of the NPY receptor have been identified in mammals, four of which are functional in humans. Subtypes Y1 and Y5 have known roles in the stimulation of feeding while Y2 and Y4 seem to have roles in appetite inhibition (satiety). Some of these receptors are among the most highly conserved neuropeptide receptors.

See also

• Anorexia nervosa
• Antianalgesia
• Neuropeptide
• Obesity

References

External links

• EMBL receptor database entry
• Neuropeptide Y at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. 膵ポリペプチド、ペプチドYY、およびニューロペプチドY pancreatic polypeptide peptide yy and neuropeptide y
• 2. グレリン ghrelin
• 3. 肥満の病因 pathogenesis of obesity
• 4. レプチンの生理学 physiology of leptin
• 5. 性腺刺激ホルモン（ゴナドトロピン）放出ホルモンの生理学 physiology of gonadotropin releasing hormone

English Journal

• Central NPY-Y5 receptors activation plays a major role in fasting-induced pituitary-thyroid axis suppression in adult rat.

• Costa-E-Sousa RH, Souza LL, Calvino C, Cabanelas A, Almeida NA, Oliveira KJ, Pazos-Moura CC.SourceBiophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, 21941-902, Rio de Janeiro, RJ, Brazil.
• Regulatory peptides.Regul Pept.2011 Nov 10;171(1-3):43-7. Epub 2011 Jul 21.
• Neuropeptide Y (NPY) inhibits TRH neurons in fed state, and hypothalamic NPY higher expression during fasting has been proposed to be involved in fasting-induced suppression of the hypothalamus-pituitary-thyroid (HPT) axis. We investigated the role of central Y5 receptors in the control of thyrotrop
• PMID 21771616

• Role of reactive oxygen species-related enzymes in neuropeptide y and proopiomelanocortin-mediated appetite control: a study using atypical protein kinase C knockdown.

• Kuo DY, Chen PN, Yang SF, Chu SC, Chen CH, Kuo MH, Yu CH, Hsieh YS.Source1 Department of Physiology, Chung Shan Medical University and Chung Shan Medical University Hospital , Taichung City, Taiwan, Republic of China .
• Antioxidants & redox signaling.Antioxid Redox Signal.2011 Oct 15;15(8):2147-59. Epub 2011 Jun 8.
• Abstract Aims: Studies have reported that redox signaling in the hypothalamus participates in nutrient sensing. The current study aimed to determine if the activation of reactive oxygen species-related enzymes (ROS-RE) in the hypothalamus participates in regulating neuropeptide Y (NPY)-mediated eati
• PMID 21453188

Japanese Journal

• 1型糖尿病の膵島関連自己抗体

• 三浦 順之助,内潟 安子,岩本 安彦
• 東京女子医科大学雑誌 81(E2), E78-E84, 2011-03-31
• … 他に抗VAMP-2 (Vesicle associated membrane protein -2)抗体、抗NPY (Neuropeptide-Y) 抗体があり、我々はそれぞれ21%、9%程度存在することを確認している。 …
• NAID 110008441448

• Hypothalamic Melanocortin System on Feeding Regulation in Birds : A Review

• BUNGO Takashi,SHIRAISHI Jun-ichi,KAWAKAMI Shin-Ichi
• The journal of poultry science 48(1), 1-13, 2011-01-25
• NAID 10027817305

Related Links

• Neuropeptide Y - Wikipedia, the free encyclopedia

"NPY has been associated with a number of physiologic processes in the brain, including the regulation of energy balance, memory and learning, and epilepsy." The main effect is increased food intake and decreased physical activity. NPY is ...

Related Pictures

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★リンクテーブル★

リンク元	「ニューロペプチドY」
拡張検索	「NPY receptor」
関連記事	「N」

「ニューロペプチドY」

　　[★]

英

neuropeptide Y NPY

• 中枢作用

血圧下降、呼吸抑制

• 末梢作用

血管収縮(冠血管含む)、血圧上昇

構造

• 36アミノ酸
• 配列は腸ホルモンの膵ポリペプチドやペプチドYYに類似する。

局在

• 細胞体

• 外側視索前野、弓状核など

• 神経終末

• 視索前野、室傍核、弓状核、視交差上核など

「NPY receptor」

　　[★]

• ニューロペプチドY受容体、ニューロペプチドYレセプター

関

neuropeptide Y receptor

「N」

　　[★]

• アスパラギン asparagine
• 窒素(原子、分子)