scholarly journals A Promising Therapeutic Target for Metabolic Diseases: Neuropeptide Y Receptors in Humans

2017 ◽  
Vol 45 (1) ◽  
pp. 88-107 ◽  
Author(s):  
Min Yi ◽  
Hekai Li ◽  
Zhiye Wu ◽  
Jianyun Yan ◽  
Qicai Liu ◽  
...  

Human neuropeptide Y (hNPY) is one of the most widely expressed neurotransmitters in the human central and peripheral nervous systems. It consists of 36 highly conserved amino acid residues, and was first isolated from the porcine hypothalamus in 1982. While it is the most recently discovered member of the pancreatic polypeptide family (which includes neuropeptide Y, gut-derived hormone peptide YY, and pancreatic polypeptide), NPY is the most abundant peptide found in the mammalian brain. In order to exert particular functions, NPY needs to bind to the NPY receptor to activate specific signaling pathways. NPY receptors belong to the class A or rhodopsin-like G-protein coupled receptor (GPCR) family and signal via cell-surface receptors. By binding to GPCRs, NPY plays a crucial role in various biological processes, including cortical excitability, stress response, food intake, circadian rhythms, and cardiovascular function. Abnormal regulation of NPY is involved in the development of a wide range of diseases, including obesity, hypertension, atherosclerosis, epilepsy, metabolic disorders, and many cancers. Thus far, five receptors have been cloned from mammals (Y1, Y2, Y4, Y5, and y6), but only four of these (hY1, hY2, hY4, and hY5) are functional in humans. In this review, we summarize the structural characteristics of human NPY receptors and their role in metabolic diseases.


2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.







Author(s):  
Y. Dumont ◽  
D. Jacques ◽  
J.-A. St-Pierre ◽  
Y. Tong ◽  
R. Parker ◽  
...  


1983 ◽  
Vol 29 (8) ◽  
pp. 1553-1554 ◽  
Author(s):  
M M O'Hare ◽  
M H Chen ◽  
K Tatemoto ◽  
K D Buchanan ◽  
S N Joffe ◽  
...  


1989 ◽  
Vol 257 (2) ◽  
pp. R383-R387 ◽  
Author(s):  
J. L. Miner ◽  
M. A. Della-Fera ◽  
J. A. Paterson ◽  
C. A. Baile

We compared the effects of neuropeptide Y (NPY) injected into the lateral ventricle (LV) and periphery (ip in rats; iv in sheep) on feed and water intake. In sated rats, a bolus injection of 1.18 or 2.35 nmol of NPY administered LV, but not ip, increased (P less than 0.05) feed intake on average of 809% within 30 min of injection. In sated sheep, an LV bolus injection of 2.35 nmol of NPY increased feed intake by 154% within 30 min. Similar doses of human pancreatic polypeptide and peptide YY were less orexigenic than NPY in sheep. After 24 h, cumulative feed intakes were similar among control and peptide treatments. Intravenous injection of 2.35 nmol NPY did not increase feed intake in sheep. Water intake was stimulated (P less than 0.05) by NPY (LV injection) in both the presence and absence of feed. We propose that NPY is involved in the central regulation of consummatory behavior in sheep.



Genomics ◽  
2000 ◽  
Vol 64 (3) ◽  
pp. 318-323 ◽  
Author(s):  
Michelle Couzens ◽  
Marjorie Liu ◽  
Camilla Tüchler ◽  
Barbara Kofler ◽  
Claudia Nessler-Menardi ◽  
...  




1993 ◽  
Vol 71 (2) ◽  
pp. 112-119 ◽  
Author(s):  
S. A. Wager-Pagé ◽  
E. Raizada ◽  
W. L. Veale ◽  
J. S. Davison

The pancreatic polypeptide-fold (PP-fold) peptides, peptide YY (PYY) and pancreatic polypeptide (PP) (200 pmol), increased duodenal intraluminal pressure following intrathecal (IT) administration into the thoracic (T8–T10) spinal cord of urethane-anesthetized rats. Neuropeptide Y (NPY), PPY, and PP (IT) increased colonic intraluminal pressure of rats. The excitatory effects of the PP-fold peptides, NPY and PYY, were accompanied by increases in mean arterial pressure (MAP) during the same time period followed by a decrease to hypotensive levels. There were no further alterations of duodenal or colonic pressure in rats during the hypotensive period. The effect of PP (IT) on MAP was characterized by a pattern of hypotension frequently followed by a hypertensive period. The modulation of duodenal and colonic pressure does not differ between the members of the PP-fold family of peptides; however, the effects of the different members of the PP-fold family of peptides on MAP were varied. The Y2 receptor ligand, NPY (13–36) (200 pmol) (IT), did not alter duodenal and colonic pressure or MAP in rats. Therefore, the effects of PYY and NPY in the thoracic spinal cord on duodenal and colonic motility may be mediated via Y1 (postjunctional) receptors. Atropine, a muscarinic antagonist, attenuated NPY's (IT) excitatory effect on colonic pressure but did not alter the MAP response to this peptide. Atropine did not modify PYY's (IT) regulation of duodenal and colonic intraluminal pressure. However, atropine did attenuate PPY's inhibitory effect on MAP. The modulatory effects of PP (IT) on colonic pressure and MAP were attenuated by atropine, suggesting that the cholinergic system may be mediating the effects of this peptide. These observations provide further evidence that the modulation of gastrointestinal motility by PYY, PP, and NPY in the thoracic spinal cord is through different mechanisms.Key words: PP-fold peptides, duodenum, colon, atropine.



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