Linked Life Data

2022633

Source:http://linkedlifedata.com/resource/pubmed/id/2022633

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1991-6-5
pubmed:abstractText
Recent evidence suggests that insulin induces hydrolysis of phosphatidylinositol-glycan (PI-G) and releases inositol-glycan (IG) and diacylglycerol (DAG). These two mediators are speculated to mediate different insulin actions. In this study, we examined metabolic labeling of PI-G in BC3H-1 myocytes with known precursors of PI-G. PI-G was metabolically labeled with [3H]myo-inositol, [3H]glucosamine, [3H]galactose, [3H]glycerol, and [3H]myristic acid. The treatment of 3H-labeled PI-G with phosphatidylinositol-specific phospholipase C liberated [3H]myo-inositol, [3H]glucosamine, or [3H]galactosamine-labeled IgGs, and [3H]glycerol or [3H]myristic acid-labeled DAG. In BC3H-1 myocytes, insulin induced phosphodiesteratic hydrolysis of PI-G and stimulated generation of IGs and DAG. Released IGs were labeled with [3H]myo-inositol, [3H]glucosamine, and [3H]galactose. Released DAG was labeled with [3H] glycerol and [3H]myristic acid. The IG had a dose-dependent insulin-like activity on glucose oxidation and lipogenesis without affecting glucose transport in rat adipocytes. Insulin increased 3H radioactivities of IG and insulin-mimicking activities of IG. These results provided further evidence that hydrolysis of PI-G and generation of IGs and DAG might be early steps in some insulin actions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8115-21
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Insulin stimulates the generation of two putative insulin mediators, inositol-glycan and diacylglycerol in BC3H-1 myocytes.
pubmed:affiliation
Third Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't