Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-10-17
pubmed:abstractText
Insulin stimulates membrane phospholipid metabolism and activates protein kinase C (PKC) in its peripheral target tissues. Additionally, insulin can stimulate PKC activity in cultured fetal chick neurons. In the present study, we tested whether insulin can stimulate membrane phospholipid metabolism in the rat hippocampus, a CNS region in which insulin has been reported to stimulate the phosphorylation of a PKC substrate protein and to suppress spontaneous electrical activity of pyramidal cells. Concentrations of 1, 10 and 100 nM insulin significantly stimulated the accumulation of [3H]inositol phosphate ([3H]IP1) and [3H]IP2 in hippocampal slices labelled with [3H]myoinositol. Significant (P less than 0.05) increases of hippocampal diacylglycerol (a product of phosphoinositol hydrolysis) content were observed at 1, 5 or 10 min of incubation with 50 or 100 nM insulin. Addition of tetrodotoxin resulted in a suppression of insulin stimulation of [3H]IP1 release, suggesting that insulin effects may be indirect and mediated via release of an endogenous neuronal transmitter within the hippocampus. Norepinephrine has been shown to both stimulate PI turnover and suppress the spontaneous electrical activity of pyramidal cells via alpha 1-adrenergic receptors. Therefore, we tested whether the effects of insulin were mediated by norepinephrine. We measured [3H]IP1 release in the presence or absence of the alpha 1-adrenergic antagonists prazobind and prazosin. These compounds blocked insulin stimulation of IP1 accumulation, suggesting that the action of insulin to stimulate PI turnover is secondary to enhancement of endogenous noradrenergic activity within the hippocampus.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Inositol, http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Lipids, http://linkedlifedata.com/resource/pubmed/chemical/Phospholipids, http://linkedlifedata.com/resource/pubmed/chemical/Prazosin, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Somatomedin, http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
550
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Insulin stimulates membrane phospholipid metabolism by enhancing endogenous alpha 1-adrenergic activity in the rat hippocampus.
pubmed:affiliation
Department of Psychology, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.