Lipoxygenase-generated icosanoids inhibit glucose-induced insulin release from rat islets
dc.contributor.author | Nathan, M. H. | en_US |
dc.contributor.author | Pek, Sumer Belbez | en_US |
dc.date.accessioned | 2006-04-10T13:44:25Z | |
dc.date.available | 2006-04-10T13:44:25Z | |
dc.date.issued | 1990-05 | en_US |
dc.identifier.citation | Nathan, M. H., Pek, S. Belbez (1990/05)."Lipoxygenase-generated icosanoids inhibit glucose-induced insulin release from rat islets." Prostaglandins, Leukotrienes and Essential Fatty Acids 40(1): 21-25. <http://hdl.handle.net/2027.42/28580> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WPH-4C305P9-4F/2/ae22250fa03303eeeabd627d64db4f0e | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/28580 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2119040&dopt=citation | en_US |
dc.description.abstract | Lipoxygenase-pathway metabolites of arachidonic acid are produced in pancreatic islets. They are are implicated in insulin release, since nonselective inhibitors of lipoxygenases inhibit glucose-induced insulin release. We studied the interplay in insulin release between glucose and selected icosanoids formed in 5-, 12- and 15-lipoxygenase pathways. Effects on immunoreactive insulin release of 107 to 10-6 12-(R)-HETE, 12-(S)-HETE, hepoxilin A3, lipoxin B4, LTB4 or LTC4 were tested individually in 30-min incubations of freshly isolated young adult Wistar rat pancreatic islets, in the presence of 5.6 mM or 23 mM glucose. Basal insulin release (at 5.6 mM glucose) was stimulated by LTC4 and hepoxilin A3 (304% and 234% of controls at 5.6 mM glucose alone, respectively), inhibited by 12-(S)-HPETE (56%), and was not affected by 12-(R)-HETE, 12-(S)-HETE, lipoxin B4 or LTB4 (111%, 105%, 106% and 136%, respectively). Insulin release evoked by 23 mM glucose (190-2-320%) was inhibited (50-145%) by all icosanoids tested, except LTC4 (162%). We conclude that, among the lipoxygenase products tested, only leukotrienes and hepoxilin are candidates for a tonic-stimulatory influence on basal insulin release. Since glucose promotes icosanoid formation in islets, the observed inhibition of glucose-induced insulin release by lipoxygenase products suggests the existence of a negative-feedback system. | en_US |
dc.format.extent | 616978 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Lipoxygenase-generated icosanoids inhibit glucose-induced insulin release from rat islets | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Chemistry | en_US |
dc.subject.hlbsecondlevel | Chemical Engineering | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Engineering | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine (Division of Endocrinology and Metabolism), University of Michigan, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationum | 5560 Medical Sciences Research Building-2, University of Michigan Medical Center, Ann Arbor, MI 48109-0678, USA | en_US |
dc.identifier.pmid | 2119040 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/28580/1/0000386.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0952-3278(90)90111-W | en_US |
dc.identifier.source | Prostaglandins, Leukotrienes and Essential Fatty Acids | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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