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• W1967086988 abstract "The initial events in signal transduction in insulin-secreting cells are summarized in FIGURE 8. Both nutrient stimuli, such as glucose and amino acids and the muscarinic agonist carbachol (carbamylcholine) raise [Ca2+]i. Although the rise in [Ca2+]i precedes the stimulation of insulin release, it is not a moment-to-moment regulator of release. The metabolizable fuel stimuli cause Ca2+ influx through voltage-dependent Ca2+ channels following depolarization of the membrane potential. In contrast, carbachol, which does not depolarize, elicits Ptd Ins 4,5-P2 hydrolysis, a reaction catalyzed by phospholipase C. The generation of Ins 1,4,5-P3 in this instance is Ca2+ independent, but appears to involve a GTP-binding protein. However, this protein is not a substrate for pertussis toxin. The levels of Ins 1,4,5-P3, which releases Ca2+ from an ATP-dependent Ca2+ pool of the endoplasmic reticulum, are increased prior to the rise in [Ca2+]i. The mitochondria may take up Ca2+ after large increases in [Ca2+]i. A previously proposed second messenger, arachidonic acid, is much less selective than Ins 1,4,5-P3 in that it releases Ca2+ from mitochondria as well as from the endoplasmic reticulum in a slow and irreversible manner. As Ins 1,4,5-P3 is also generated during glucose stimulation of islets, albeit in a Ca2+-dependent manner, this metabolite could mediate not only the action of carbachol but also contribute to amplifying the [Ca2+]i rise in response to glucose." @default.
• W1967086988 created "2016-06-24" @default.
• W1967086988 creator A5025783423 @default.
• W1967086988 creator A5072228093 @default.
• W1967086988 date "1986-12-01" @default.
• W1967086988 modified "2023-10-09" @default.
• W1967086988 title "Signal Transduction in Insulin Secretion:." @default.
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• W1967086988 doi "https://doi.org/10.1111/j.1749-6632.1986.tb46568.x" @default.
• W1967086988 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/3107454" @default.
• W1967086988 hasPublicationYear "1986" @default.
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