Linked Life Data

10426371

Source:http://linkedlifedata.com/resource/pubmed/id/10426371

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1999-8-11
pubmed:abstractText
Glucose augments Ca2+-stimulated insulin release from the pancreatic beta-cell in an ATP-sensitive K+ channel (K(ATP) channel)-independent manner. In studying the mechanisms underlying this action, we used rat pancreatic islets and examined the effects of exogenous free fatty acids (FFAs), which are precursors of long-chain acyl-CoA (LC-CoA), on KCl-induced Ca2+-stimulated insulin release. Myristate, palmitate, and stearate augmented insulin release induced by 50 mmol/l KCl in the presence of 2.8 mmol/l glucose. Added acutely, their potency was weak compared with that of glucose-induced augmentation. The FFA-induced augmentation became much greater, however, when islets were preincubated with FFAs under stringent Ca2+-free conditions (with 1 mmol/l EGTA) before the KCl stimulation. Under these conditions, 16.7 mmol/l glucose augmented 13-fold insulin release induced by 50 mmol/l KCl, whereas palmitate or myristate (both at a free concentration of 10 micromol/l) produced 5.8- and 5.2-fold augmentations. Effects of FFAs and glucose were concentration-dependent. The temporal profiles of augmentation induced by 11.1 mmol/l glucose and 10 micromol/l palmitate were similar. Glucose and palmitate caused almost identical augmentation patterns for the initial 10 min of stimulation; subsequently, glucose augmentation was better sustained than palmitate augmentation. This suggests the existence of a longer-term glucose-specific signaling moiety that cannot be mimicked by FFAs. Our results provide direct evidence that FFAs can mimic the K(ATP) channel-independent action of glucose. Taking these results together with previous results, we conclude that glucose augments Ca2+-stimulated insulin release, at least in part, by increasing malonyl-CoA and cytosolic LC-CoA. However, one or more other glucose-specific signaling molecules are required for the full expression of augmentation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Diazoxide, http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations, http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified, http://linkedlifedata.com/resource/pubmed/chemical/Glucose, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Myristic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Palmitic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1543-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10426371-Adenosine Triphosphate, pubmed-meshheading:10426371-Animals, pubmed-meshheading:10426371-Calcium, pubmed-meshheading:10426371-Diazoxide, pubmed-meshheading:10426371-Drug Combinations, pubmed-meshheading:10426371-Extracellular Space, pubmed-meshheading:10426371-Fatty Acids, pubmed-meshheading:10426371-Fatty Acids, Nonesterified, pubmed-meshheading:10426371-Glucose, pubmed-meshheading:10426371-Insulin, pubmed-meshheading:10426371-Islets of Langerhans, pubmed-meshheading:10426371-Male, pubmed-meshheading:10426371-Myristic Acid, pubmed-meshheading:10426371-Palmitic Acid, pubmed-meshheading:10426371-Potassium Channels, pubmed-meshheading:10426371-Potassium Chloride, pubmed-meshheading:10426371-Rats, pubmed-meshheading:10426371-Rats, Wistar, pubmed-meshheading:10426371-Time Factors
pubmed:year
1999
pubmed:articleTitle
Augmentation of Ca2+-stimulated insulin release by glucose and long-chain fatty acids in rat pancreatic islets: free fatty acids mimic ATP-sensitive K+ channel-independent insulinotropic action of glucose.
pubmed:affiliation
Department of Aging Medicine and Geriatrics, Shinshu University School of Medicine, Matsumoto, Japan. mitsu@neco.or.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't