scholarly journals Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice

Aging ◽  
2020 ◽  
Vol 12 (14) ◽  
pp. 13939-13957
Author(s):  
Emanuela Agosti ◽  
Marilisa De Feudis ◽  
Elia Angelino ◽  
Roberta Belli ◽  
Maraiza Alves Teixeira ◽  
...  
Keyword(s):  
Nutrition ◽  
2021 ◽  
Vol 87-88 ◽  
pp. 111316
Author(s):  
G. Gortan Cappellari ◽  
A. Semolic ◽  
G. Cremasco ◽  
P. Vinci ◽  
M. Zanetti ◽  
...  

2014 ◽  
Vol 17 (3) ◽  
pp. 236-240 ◽  
Author(s):  
Simone Reano ◽  
Andrea Graziani ◽  
Nicoletta Filigheddu

2016 ◽  
Author(s):  
Gabrielle Crisp ◽  
Ohn Nyunt ◽  
Lisa Chopin ◽  
Inge Seim ◽  
Mark Harris ◽  
...  

AbstractPrader-Willi Syndrome (PWS) is a complex genetic disorder characterized by developmental and growth abnormalities, insatiable appetite, and excessive eating (hyperphagia). The underlying cause of hyperphagia in PWS is currently unknown, however, elevated levels of the peptide hormone ghrelin is believed to contribute. Recently, ghrelin-reactive autoantibodies (isotype IgG) were identified in non-genetic obesity. These autoantibodies act as ghrelin carrier proteins and potentiate its orexigenic effects. Here, we describe the identification of ghrelin-reactive autoantibodies in a cohort of 16 children with PWS. In comparison to unaffected siblings, autoantibody levels are significantly increased in PWS children. We further show that autoantibody levels are unaffected by food intake, unlike plasma ghrelin which declines postprandially in both groups. Critically, we also demonstrate that the autoantibodies bind the major circulating ghrelin isoforms, unacylated ghrelin, which does not stimulate appetite, and the orexigen acylated ghrelin. In excess, unacylated ghrelin may compete with acylated ghrelin for autoantibody binding. Taken together, this is the first report on ghrelin-reactive antibodies in a pediatric population, and the first to demonstrate that the antibodies do not discriminate between orexigenic and non-orexigenic ghrelin isoforms. Our work suggests that ghrelin autoantibodies can be targeted using non-orexigenic forms of ghrelin, thereby providing a novel therapeutic target for PWS and for obesity in general.


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
David Huynh ◽  
Valerie Bessi ◽  
Liliane Ménard ◽  
Christophe Noll ◽  
Andre Carpentier ◽  
...  

2020 ◽  
Vol 63 (5) ◽  
pp. 195
Author(s):  
Sizeng Chen ◽  
Xianliang Zeng ◽  
Ping Chen ◽  
Li Zhao

2019 ◽  
Vol 20 (3) ◽  
pp. 499 ◽  
Author(s):  
Michela Zanetti ◽  
Gianluca Gortan Cappellari ◽  
Andrea Graziani ◽  
Rocco Barazzoni

Unacylated ghrelin (UnGhr) exerts several beneficial actions on vascular function. The aim of this study was to assess the effects of UnGhr on high-fat induced endothelial dysfunction and its underlying mechanisms. Thoracic aortas from transgenic mice, which were overexpressing UnGhr and being control fed either a standard control diet (CD) or a high-fat diet (HFD) for 16 weeks, were harvested and used for the assessment of vascular reactivity, endothelial nitric oxide synthase (eNOS) expression and activity, thiobarbituric acid reactive substances (TBARS) and glutathione levels, and aortic lipid accumulation by Oil Red O staining. Relaxations due to acetylcholine and to DEA-NONOate were reduced (p < 0.05) in the HFD control aortas compared to vessels from the CD animals. Overexpression of UnGhr prevented HFD-induced vascular dysfunction, while eNOS expression and activity were similar in all vessels. HFD-induced vascular oxidative stress was demonstrated by increased (p < 0.05) aortic TBARS and glutathione in wild type (Wt) mice; however, this was not seen in UnGhr mice. Moreover, increased (p < 0.05) HFD-induced lipid accumulation in vessels from Wt mice was prevented by UnGhr overexpression. In conclusion, chronic UnGhr overexpression results in improved vascular function and reduced plaque formation through decreased vascular oxidative stress, without affecting the eNOS pathway. This research may provide new insight into the mechanisms underlying the beneficial effects of UnGhr on the vascular dysfunction associated with obesity and the metabolic syndrome.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Elia Angelino ◽  
Simone Reano ◽  
Michele Ferrara ◽  
Emanuela Agosti ◽  
Andrea Graziani ◽  
...  

Fibrosis can affect almost all tissues and organs, it often represents the terminal stage of chronic diseases, and it is regarded as a major health issue for which efficient therapies are needed. Tissue injury, by inducing necrosis/apoptosis, triggers inflammatory response that, in turn, promotes fibroblast activation and pathological deposition of extracellular matrix. Acylated and unacylated ghrelin are the main products of the ghrelin gene. The acylated form, through its receptor GHSR-1a, stimulates appetite and growth hormone (GH) release. Although unacylated ghrelin does not bind or activate GHSR-1a, it shares with the acylated form several biological activities. Ghrelin peptides exhibit anti-inflammatory, antioxidative, and antiapoptotic activities, suggesting that they might represent an efficient approach to prevent or reduce fibrosis. The aim of this review is to summarize the available evidence regarding the effects of acylated and unacylated ghrelin on different pathologies and experimental models in which fibrosis is a predominant characteristic.


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