NPY

Official Full Name

neuropeptide Y

Organism

Homo sapiens

GeneID

4852

Background

This gene encodes a neuropeptide that is widely expressed in the central nervous system and influences many physiological processes, including cortical excitability, stress response, food intake, circadian rhythms, and cardiovascular function. The neuropeptide functions through G protein-coupled receptors to inhibit adenylyl cyclase, activate mitogen-activated protein kinase (MAPK), regulate intracellular calcium levels, and activate potassium channels. A polymorphism in this gene resulting in a change of leucine 7 to proline in the signal peptide is associated with elevated cholesterol levels, higher alcohol consumption, and may be a risk factor for various metabolic and cardiovascular diseases. The protein also exhibits antimicrobial activity against bacteria and fungi. [provided by RefSeq, Oct 2014]

Synonyms

PYY4;

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Detailed Information

Neuropeptide Y (NPY) is widely distributed in various parts of the body, but mainly exists in sympathetic nerve endings and has a strong vasoconstrictor effect. It exerts a biological effect by combining with receptors and is an important substance for regulating vasoconstriction and relaxation. In recent years, many scholars have conducted various studies on NPY, and found that NPY plays an important role in the occurrence, development and prognosis of the main system diseases of the human body.

Npy Figure 1. Intracellular signaling cascades for Neuropeptide Y receptors. (Tan, C. M. J., et al. 2018)

The Features of NPY

The structure of NPY is similar to that of pancreatic polypeptide and YY peptide, with a total of 36 amino acid residues. NPY is widely distributed in various tissues and organs in the central nervous system and periphery, and is related to learning, memory, convulsions, pain, anxiety, depression, and food intake. NPY mainly exists in sympathetic nerve endings, and its function is similar to that of norepinephrine, and it is released together with it. It acts as a neurotransmitter or modulator and exerts physiological regulation. NPY in the blood is partly derived from sympathetic nerves and partly derived from platelets, and is released during sympathetic nerve excitation and platelet aggregation.

NPY mainly functions by binding to receptors. NPY receptors include subtypes Y1, Y2, Y3, Y4, Y5, Y6, Y7, and Y8, among which Y1 and Y2 are key receptors and are abundantly expressed in vascular smooth muscle. In addition to its powerful vasoconstriction effect, NPY can also cause calcium homeostasis changes, cardiomyocyte hypertrophy, ischemia-induced vascular remodeling, protein kinase C signal transduction, and regulation of the renin-angiotensin-aldosterone system.

NPY and Coronary Heart Disease

Coronary heart disease is mainly caused by stenosis or occlusion of atherosclerosis, which leads to myocardial ischemia and is affected by many factors. In recent years, studies have found that sympathetic nerve excitation can produce NPY, which can promote the formation of coronary atherosclerosis, the main mechanism is related to vasoconstrictor effect, platelet activation and insulin resistance. The occurrence of acute coronary syndrome is associated with acute thrombosis and coronary vasospasm.

The study found that the increase in plasma NPY levels in patients with acute myocardial infarction and unstable angina may be partly due to the release of platelets. The initial step of thrombosis is platelet aggregation. When coronary artery endothelium is injured, NPY can accumulate at the platelet aggregation site and activate platelets. Platelet aggregation and release NPY. With the increase of NPY level, it can also cause coronary artery spasm. Increasing the blood perfusion around the area of myocardial infarction can reduce the area of myocardial infarction, and the level of NPY released by nerve endings in the area of myocardial infarction due to the vasoconstriction effect of NPY and myocardial infarction further increases. This further reduces the blood flow in the area of the infarct and enlarges the area of myocardial infarction.

Npy and Other Diseases

As a nerve mediator with vascular activity, NPY is widely distributed in the sympathetic nerve endings, which can further accelerate heart rate and increase heart failure. Some scholars believe that plasma NPY levels increase significantly in patients with congestive heart failure, and change with changes in cardiac function, which can be used as a reference index for evaluating the severity and prognosis of patients with congestive heart failure. By observing the NPY level of patients with cerebral infarction at different degrees, it was found that the plasma NPY level of patients with cerebral infarction was significantly increased. The infarct severity is higher than the mild one, the infarct lesion is larger than the small lesion, and the infarction with hypertension is higher than that without hypertension. Therefore, NPY can be used as a non-specific indicator of the severity of cerebral infarction.

References:

Tan, C. M. J. , Green, P. , Tapoulal, N. , Lewandowski, A. J. , Leeson, P. , & Herring, N. . (2018). The role of neuropeptide y in cardiovascular health and disease. Frontiers in Physiology, 9.
Lu, L. , Zou, Y. C. , Wang, M. , Huang, Y. F. , Chen, D. X. , & Wei, L. B. . (2015). Neuropeptide y levels are associated with nutritional status and cardiovascular events in adults with chronic kidney disease. European Journal of Clinical Nutrition,69(6), 717-721.
FehÃ©r E. (2015). [changes in neuropeptide y and substance p immunoreactive nerve fibres and immunocompetent cells in hepatitis]. orv hetil, 135(1), 1892-1897.

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