Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-12-12
pubmed:abstractText
AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. Changes in AMPK activity contribute to the regulation of insulin secretion. Epidemiological evidence links the ingestion of saturated fatty acid with hyperinsulinemia. The aim of the present study was to examine the effects of palmitate on beta cell AMPK activity and insulin secretion. Isolated rat islets and MIN6 beta cells were treated acutely (5-60 min) or chronically (24 h) with palmitate. Insulin secretion, AMPK and acetyl CoA carboxylase phosphorylation were assessed. The acute effects of palmitate included AMPK activation and augmentation in insulin secretion. Activation of AMPK by 24h pretreatment with palmitate suppressed glucose-stimulated insulin secretion, but not the response of insulin secretion to combined stimuli of glucose and palmitate. This study demonstrated that palmitate availability affected beta cell AMPK activity. In beta cells, an increase in AMPK activity may be required for fatty acid-induced fatty acid oxidation and prevention of lipotoxicity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
352
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
463-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Palmitate activates AMP-activated protein kinase and regulates insulin secretion from beta cells.
pubmed:affiliation
Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't