Signal transduction in XXXX secretion: comparison between fuel stimuli and receptor agonists.

@entity1522 @entity15055 @entity2690 @entity1426 @entity413 @entity141 @entity5402 @entity855
The initial events in signal transduction in @entity2690 -secreting cells are summarized in FIGURE 8. Both nutrient stimuli, such as @entity413 and @entity1522 and the muscarinic agonist @entity5402 ( @entity5402 ) raise [ @entity141 ]i. Although the rise in [ @entity141 ]i precedes the stimulation of @entity2690 release, it is not a moment-to-moment regulator of release. The metabolizable fuel stimuli cause @entity141 influx through voltage-dependent @entity141 channels following depolarization of the membrane potential. In contrast, @entity5402 , 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 @entity141 independent, but appears to involve a @entity15055 . However, this protein is not a substrate for pertussis toxin. The levels of Ins 1,4,5-P3, which releases @entity141 from an @entity855 -dependent @entity141 pool of the endoplasmic reticulum, are increased prior to the rise in [ @entity141 ]i. The mitochondria may take up @entity141 after large increases in [ @entity141 ]i. A previously proposed second messenger, @entity1426 , is much less selective than Ins 1,4,5-P3 in that it releases @entity141 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 @entity413 stimulation of islets, albeit in a @entity141 -dependent manner, this metabolite could mediate not only the action of @entity5402 but also contribute to amplifying the [ @entity141 ]i rise in response to @entity413 .
