Linked Life Data

623294

Source:http://linkedlifedata.com/resource/pubmed/id/623294

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1978-3-29
pubmed:abstractText
The ability of large fat cells from spontaneously obese rats to synthesize fatty acids from D-[1-14C]glucose, D-[6-14C]glucose, or [2-14C]pyruvate was markedly diminished compared to small fat cells from lean animals. Furthermore, fatty acid synthetase and acetyl coenzyme A carboxylase activities in dialyzed homogenates of large fat cells were inhibited by 84 and 90%, respectively, compared to small cells. Pentose shunt activity, but not glycolytic flux, was also markedly inhibited in large fat cells incubated with or without insulin. However, the NADPH oxidant vitamin K5 completely restored pentose shunt activity in large cells to the elevated levels observed in small fat cells in the presence of this agent or insulin. Furthermore, inhibition of mitochondrial oxidation and fatty acid synthesis in small cells by rotenone led to a secondary inhibition of pentose shunt activity indicating a link between these two pathways. Direct measurements of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities in fat cell homogenates showed no difference between cell types. The data provide strong support for the hypothesis that the fatty acid synthetic pathway is the primary metabolic defect in large insulin-resistant rat adipocytes, a defect which secondarily leads to inhibited pentose shunt activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
234
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E182-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1978
pubmed:articleTitle
Primary role of decreased fatty acid synthesis in insulin resistance of large rat adipocytes.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.