About: A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma

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About: A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma
Creator	Cao, Hong Alexander, · Bhaskar Kallakury, · Ciofoaia, · Gay, Martha Huber, · Kroemer, H Kruger, Annie Narayan Shivapurkar, · Safronenka, Anita Sandeep Nadella, · Smith, Jill Tucker, Robin
source	PMC
abstract	BACKGROUND AND AIMS: Nonalcoholic steatohepatitis (NASH) is a common inflammatory liver condition that may lead to cirrhosis and hepatocellular carcinoma (HCC). Risk factors for NASH include a saturated fat diet, altered lipid metabolism, and genetic and epigenetic factors, including microRNAs. Serum levels of cholecystokinin (CCK) are elevated in mice and humans that consume a high-saturated fat diet. CCK receptors (CCK-Rs) have been reported on fibroblasts which when activated can induce fibrosis; however, their role in hepatic fibrosis remains unknown. We hypothesized that elevated levels of CCK acting on the CCK-Rs play a role in the development of NASH and in NASH-associated HCC. METHODS: We performed a NASH Prevention study and Reversal study in mice fed a saturated fat 75% choline-deficient–ethionine-supplemented (CDE) diet for 12 or 18 weeks. In each study, half of the mice received untreated drinking water, while the other half received water supplemented with the CCK-R antagonist proglumide. CCK-R expression was evaluated in mouse liver and murine HCC cells. RESULTS: CCK receptor antagonist treatment not only prevented NASH but also reversed hepatic inflammation, fibrosis, and steatosis and normalized hepatic transaminases after NASH was established. Thirty-five percent of the mice on the CDE diet developed HCC compared with none in the proglumide-treated group. We found that CCK-BR expression was markedly upregulated in mouse CDE liver and HCC cells compared with normal hepatic parenchymal cells, and this expression was epigenetically regulated by microRNA-148a. CONCLUSION: These results support the novel role of CCK receptors in the pathogenesis of NASH and HCC.
has issue date	2019-07-11(xsd:dateTime)
bibo:doi	10.1007/s10620-019-05722-3
bibo:pmid	31297627
has license	no-cc
sha1sum (hex)	bb1ec6ec0eb08408c450859d3e9d1427a84abc4c
schema:url	https://doi.org/10.1007/s10620-019-05722-3
resource representing a document's title	A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma
has PubMed Central identifier	PMC6946881
has PubMed identifier	31297627
schema:publication	Dig Dis Sci
resource representing a document's body	covid:bb1ec6ec0eb08408c450859d3e9d1427a84abc4c#body_text
is schema:about of	named entity 'CCK' named entity 'proglumide' named entity 'NASH' named entity 'CCK' named entity 'reversed' named entity 'hypothesized' named entity 'Cholecystokinin' named entity 'THESE' named entity 'ACTING' named entity 'CONDITION' named entity 'MARKEDLY' named entity 'HALF' named entity 'EPIGENETIC' named entity 'LEVELS' named entity 'CCK-BR' named entity 'parenchymal cells' named entity 'cholecystokinin' named entity 'diet' named entity 'lipid metabolism' named entity 'microRNAs' named entity 'levels' named entity 'hepatic' named entity 'HCC' named entity 'mice' named entity 'regulated' named entity 'expression' named entity 'saturated fat' named entity 'liver' named entity 'hepatic' named entity 'HCC' named entity 'transaminases' named entity 'NASH' named entity 'Serum levels' named entity 'parenchymal cells' named entity 'fibroblasts' named entity 'NASH' named entity 'epigenetic factors' named entity 'fibrosis' named entity 'NASH' named entity 'Antagonist' named entity 'HCC' named entity 'gut microbiome' named entity 'NASH' named entity 'cell lines' named entity 'denaturation' named entity 'CCK' named entity 'densitometry' named entity 'liver tissue' named entity 'receptor' named entity 'denaturation' named entity 'anti-fibrotic' named entity 'gastric cancer' named entity 'body weight' named entity 'mice' named entity 'NASH' named entity 'FAP' named entity 'mice' named entity 'mice' named entity 'mice' named entity 'treatment group' named entity 'fibrosis' named entity 'strong safety' named entity 'Gaithersburg' named entity 'mice' named entity 'fibrosis' named entity 'AST' named entity 'Thermo Scientific' named entity 'fibrosis' named entity 'CCK'

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