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About:
GHSR-1a is not Required for Ghrelin’s Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia
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schema:ScholarlyArticle
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covidontheweb.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
GHSR-1a is not Required for Ghrelin’s Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia
Creator
Anderson, Barbara
Hernandez,
Garcia, Jose
Chen, Ji-An
Guillory, Bobby
Lee, In-Gi
Liu, Haiming
Luo, Jiaohua
Storie, Mackenzie
Tewnion, Alison
Yoeli, Jordan
Zang, Pu
Source
BioRxiv
abstract
Adipose tissue (AT) atrophy is a hallmark of cancer cachexia contributing to increased morbidity/mortality. Ghrelin has been proposed as a treatment for cancer cachexia partly by preventing AT atrophy. However, the mechanisms mediating ghrelin’s effects are incompletely understood, including the extent to which its only known receptor, GHSR-1a, is required for these effects. This study characterizes the pathways involved in AT atrophy in the Lewis Lung Carcinoma (LLC)-induced cachexia model and those mediating the effects of ghrelin in Ghsr+/+ and Ghsr−/− mice. We show that LLC causes AT atrophy by inducing anorexia, and increasing AT inflammation, thermogenesis and energy expenditure. These changes were greater in Ghsr−/−. Ghrelin administration prevented LLC-induced anorexia only in Ghsr+/+, but prevented WAT inflammation and atrophy in both genotypes, although its effects were greater in Ghsr+/+. LLC-induced increases in BAT inflammation, WAT and BAT thermogenesis, and energy expenditure were not affected by ghrelin. In conclusion, ghrelin ameliorates WAT inflammation, fat atrophy and anorexia in LLC-induced cachexia. GHSR-1a is required for ghrelin’s orexigenic effect but not for its anti-inflammatory or fat-sparing effects.
has issue date
2019-12-06
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)
bibo:doi
10.1101/866376
has license
biorxiv
sha1sum (hex)
45a70ea95db85019f402958714218a2de2aab676
schema:url
https://doi.org/10.1101/866376
resource representing a document's title
GHSR-1a is not Required for Ghrelin’s Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia
schema:publication
bioRxiv
resource representing a document's body
covid:45a70ea95db85019f402958714218a2de2aab676#body_text
is
schema:about
of
named entity 'Fat'
named entity 'significant effect'
named entity 'Cachexia'
named entity 'SPSS'
named entity 'Ghsr'
named entity 'inflammation'
named entity 'Fat'
named entity 'GHSR'
named entity 'tumor'
named entity 'food intake'
named entity 'tumor'
named entity 'phosphate buffered saline'
named entity 'Laboratory Animal'
named entity 'GHSR'
named entity 'WAT'
named entity 'GHSR'
named entity 'tumor'
named entity 'inflammation'
named entity 'Tumor'
named entity 'tumor'
named entity 'inflammation'
named entity 'mice'
named entity 'lipolysis'
named entity 'WAT'
named entity 'BAT'
named entity 'mice'
named entity 'BAT'
named entity 'congenic'
named entity 'significant source'
named entity 'mice'
named entity 'upregulation'
named entity 'lipogenesis'
named entity 'IL-6'
named entity 'survival rates'
named entity 'Manassas'
named entity 'ghrelin'
named entity 'macrophages'
named entity 'microscope'
named entity 'endothelial cells'
named entity 'carbon dioxide'
named entity 'energy expenditure'
named entity 'statistical analysis'
named entity 'growth hormone'
named entity 'receptor'
named entity 'randomized, placebo-controlled'
named entity 'Weight loss'
named entity 'osmotic'
named entity 'macrophage'
named entity 'IL-6'
named entity 'BAT'
named entity 'VWR'
named entity 'LLC'
named entity 'cytokine'
named entity 'tumor'
named entity 'mechanisms of action'
named entity 'F4/80'
named entity 'GHSR'
named entity 'adipose tissue'
named entity 'ghrelin'
named entity 'Cryostat'
named entity 'primary antibodies'
named entity 'lipolysis'
named entity 'IL-1β'
named entity 'cytokines'
named entity 'physical activity'
named entity 'gavage'
named entity 'anorexia'
named entity 'energy expenditure'
named entity 'LLC'
named entity 'IBM'
named entity 'ghrelin'
named entity 'American Type Culture Collection'
named entity 'IL-6'
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