Linked Life Data

2519840

Source:http://linkedlifedata.com/resource/pubmed/id/2519840

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-3-9
pubmed:abstractText
The growth of Ehrlich ascites tumors (EAT) in mice induces hypertriglyceridemia and depletion of lipid stores. H-Riop: Swiss mice in early and late stages of tumor growth were examined to investigate whether an increase in liver synthesis of fatty acids (FA) and/or an increase in the liver triglyceride (TG) secretion rates (TGSR) would contribute to endogenous cancer-induced hypertriglyceridemia. Using 3H2O as tracer, FA synthesis decreased in the liver of tumorous animals. Hepatic TGSR also decreased during the development of hypertriglyceridemia. On the basis of these results, hypertriglyceridemia is probably not due to hyperproduction of lipids by the liver. In the late stage of tumor growth a considerable drop of FA synthesis also ensued in the adipose tissues, which probably participated in the loss of carcass lipids. At the early stage of tumor growth FA synthesis in the EAT cells was substantial in relation to the low lipid content of these cells, but in the late period FA synthesis slowed down, indicating that the triglyceride-rich "older" tumor cells obtained a large part of their lipids performed by the host.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0258-851X
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-33
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:articleTitle
Changes in the rates of lipogenesis and hepatic triglyceride secretion in mice bearing Ehrlich ascites carcinoma.
pubmed:affiliation
National Institute of Oncology, Budapest, Hungary.
pubmed:publicationType
Journal Article