Linked Life Data

10094957

Source:http://linkedlifedata.com/resource/pubmed/id/10094957

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-5-20
pubmed:abstractText
Fatty liver is common in nonalcoholic, obese individuals and in lean people who consume alcohol chronically. Although fatty liver is typically benign, a subset of individuals with steatosis develop steatohepatitis and eventually cirrhosis. The disparate outcomes of fatty liver suggest that it reflects a generally beneficial, adaptive response to obesity or alcohol-related stress, but may also increase hepatocyte vulnerability to other challenges. Thus, both protective factors (e.g., Bcl-2 and Bcl-xL) and factors that promote hepatocyte death by apoptosis (e.g., Bax) or necrosis (e.g., UCP2) may be increased in fatty livers. To evaluate this possibility, hepatocyte apoptosis, necrosis, and the expression of factors that regulate cellular viability were assessed in two models of fatty liver (i.e., genetically obese [ob/ob] mice and ethanol [EtOH]-fed lean mice). Findings in mice with fatty livers were compared with lean, control mice that did not have hepatic steatosis. Immunohistochemistry showed striking induction of hepatocyte proteins that promote (e.g., Bax) and inhibit (e.g., Bcl-2 and Bcl-xL) apoptosis in both groups with fatty liver. Both models of fatty liver also increased hepatic transcripts for UCP2, a mitochondrial uncoupling protein, and the protein itself was induced in ob/ob hepatocytes. Despite the up-regulation of factors that threaten cell viability, hepatocyte death was not increased in either ob/ob or EtOH-fed mice, confirming that the liver's protective responses were sufficient under the conditions studied. However, if UCP2 induction reduces the efficiency of adenosine triphosphate (ATP) synthesis, this initially harmless response might enhance the vulnerability of hepatocytes to necrosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1131-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10094957-Animals, pubmed-meshheading:10094957-Apoptosis, pubmed-meshheading:10094957-Blotting, Northern, pubmed-meshheading:10094957-Fatty Liver, pubmed-meshheading:10094957-Fatty Liver, Alcoholic, pubmed-meshheading:10094957-Immunohistochemistry, pubmed-meshheading:10094957-In Situ Nick-End Labeling, pubmed-meshheading:10094957-Ion Channels, pubmed-meshheading:10094957-Male, pubmed-meshheading:10094957-Membrane Transport Proteins, pubmed-meshheading:10094957-Mice, pubmed-meshheading:10094957-Mice, Inbred C57BL, pubmed-meshheading:10094957-Mice, Obese, pubmed-meshheading:10094957-Mitochondria, pubmed-meshheading:10094957-Mitochondrial Proteins, pubmed-meshheading:10094957-Necrosis, pubmed-meshheading:10094957-Obesity, pubmed-meshheading:10094957-Proteins, pubmed-meshheading:10094957-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:10094957-RNA, pubmed-meshheading:10094957-Uncoupling Agents
pubmed:year
1999
pubmed:articleTitle
Mitochondrial proteins that regulate apoptosis and necrosis are induced in mouse fatty liver.
pubmed:affiliation
Department of Pathology, Johns Hopkins University, Baltimore, MD, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.