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Título del libro: Ghrelin: Function, Mechanism Of Action And Role In Health And Disease
Título del capítulo: The role of ghrelin in vascular tone regulation in relationship with oxidative stress and lipids

Autores UNAM:
MIGUEL ANGEL DIAZ FLORES; ADOLFO JOSE CHAVEZ NEGRETE;
Autores externos:

Idioma:

Año de publicación:
2019
Palabras clave:

Endothelial dysfunction; Ghrelin; Obesity; Oxidative stress; Vascular


Resumen:

Adiposity and insulin resistance in adipose tissues are pathognomonic to obesity. Also, the development of obesity contributes to the unbalanced production of pro-inflammatory and anti-inflammatory adipokines in white adipose tissue (WAT). Obesity is the cause of several pathologies that increase the risk of complications and health costs worldwide.In recent years, interest in homeostasis between appetite and body weight has increased. The regulation of appetite and food intake is highly complex and the participation of different hormones is key to understanding the origin of obesity and its complications. One of these hormones is ghrelin, discovered in 1999 as a ligand for growth hormone. It is a 28-amino acid peptide, an orexigenic hormone that is secreted primarily by the stomach and duodenum and has been implicated in both mealtime hunger and the long-term regulation of body weight. Ghrelin is also structurally unique, requiring post-translational acylation of the third (serine) residue to enable it to bind to and activate its cognate receptor, the growth hormone secretagogue receptor, GHS-R1a. This modification is accomplished by the action of ghrelin O-acyl transferase (GOAT), a member of the membrane-bound O-acyl transferase (MBOAT) family of enzymes. The role of ghrelin/GHS-R (GHS receptor) signaling in systemic inflammation is controversial; both proinflammatory and anti-inflammatory effects have been reported. Although ghrelin has been shown to have anti-inflammatory effects, it has also been shown to be involved inseveral physiological processes, including growth hormone (GH) release stimulation, energy balance induction, and vascular tone regulation. Zhao et al. proved that in cardiovascular dysfunction, characterized by reduced cardiac contractility and depressed endotheliumdependent vascular relaxation, ghrelin could regulate vascular endothelial cell function through inhibition of vascular endothelial cell apoptosis. Also, in previous reports, it demonstrates the effects of unacylated ghrelin upregulation on vascular tone and oxidative stress in a transgenic model, as well as the systemic circulating unacylated ghrelin upregulation and high-fat diet-induced obesity on the vascular response. Unacylated ghrelin in different species has been researched instudies about vascular districts and disease states. Collectively, the majority of these studies have shown that unacylated ghrelin evokes endothelium-dependent dilation. The endothelial dysfunction (ED) is characterized by impaired endothelial-dependent relaxation, aberrant oxidative stress, and enhanced cell apoptosis which is attributed to high levels of reactive oxygen species (ROS), diminished endothelial antioxidant defense, and ROS scavenging of nitric oxide (NO). ED is also a main risk factor for the development of cardiovascular diseases (CVD). On the other hand, studies have reported that decrease of ghrelin level may contribute to ED and development of atherosclerosis. However, in actuality it has been shown that ghrelin exerts cardiac protective effects, such as protection from ischemia/reperfusion injury and attenuation of left ventricular remodeling following myocardial infarction. However, new findings involved adipose tissue lipolysis and lipid uptake are critical for activation of macrophages. These findings highlight the ghrelin system as a promising candidate for cardiovascular drug discovery and may be a new therapeutic approach to the treatment of endothelial impairment and may contribute to the prevention of atherosclerosis. © 2020 by Nova Science Publishers, Inc. All rights reserved.


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