Linked Life Data

1682135

Source:http://linkedlifedata.com/resource/pubmed/id/1682135

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-12-2
pubmed:abstractText
The sites of action for somatostatin and epinephrine to inhibit insulin secretion have been reported to be exclusively in the exocytotic pathway. We used HIT cells, a clonal line of beta-cells, to examine whether these hormones might have as yet undescribed, nonexocytotic effects on insulin messenger RNA levels. We observed that both somatostatin and epinephrine not only inhibit insulin secretion (53 +/- 2% and 50 +/- 2% of control, respectively) but also decrease insulin mRNA levels (54 +/- 5% and 66 +/- 5% of control, respectively) and insulin content in HIT cells (61 +/- 2% and 51 +/- 1% of control, respectively). The latter two effects are discernible by 24 h, maximal by 48 h, and are prevented by preincubation of HIT cells with pertussis toxin. These new observations suggest that somatostatin and epinephrine negatively modulate insulin availability through a guanine nucleotide binding protein-mediated step in insulin synthesis before the exocytotic pathway. This general mechanism may allow these two hormones to serve as more long-term regulators of insulin availability in distinction to their shorter term and more readily reversible inhibitory effects on the exocytotic pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
129
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2409-14
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Somatostatin and epinephrine decrease insulin messenger ribonucleic acid in HIT cells through a pertussis toxin-sensitive mechanism.
pubmed:affiliation
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.