The results suggest that the Ca2+-dependent breakdown of polyphosphoinositides in an early metabolic event during the initiation of insulin release
2015
Key concepts
Scholarcy highlights
- Isolated islets were incubated withP1 and radiolabelling of polyphosphoinositides were determined
- The results show that catabolism of islet polyphosphoinositides is responsive to various stimuli of insulin secretion
- The spots containing the polyphosphoinositides remained as single spots and retained the level of radioactivity obtained after one-dimensional development when the plates were subsequently developed in a second-dimension using the solvent system chloroform/methanol/acetic acid/water
- D-galactose, which is not a secretagogue in islets, did not show the polyphosphoinositide effect characterized by glucose stimulation
- The effects of glucose on the breakdown of islet polyphosphoinositides were modulated by Ca2, since the inhibition of lipid breakdown by the Ca2+-chelating agent EGTA was partially reversed by Ca2+ addition
- The present studies demonstrating that insulin secretagogues provoke the breakdown of polyphosphoinositides are reminiscent of a similar phospholipid effect in other secretory cells
Need more features? Save interactive summary cards to your Scholarcy Library.