1983
DOI: 10.1042/bj2160101
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Isolated islets were incubated with [32P]P1 and radiolabelling of polyphosphoinositides were determined. Labelling equilibrium was approached after 45 min, with a half-time of 15 min. D-Glucose decreased the amount of [32P]PO4 in phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] and phosphatidylinositol 4-phosphate (PtdIns4P) within 0.5 min, and loss of radiolabel was still evident at 1 min. [32P]PO4 levels in polyphosphoinositides returned to basal levels within 5 min. Neither D-galactose nor D-glucose af… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

4
37
1

Year Published

1985
1985
2009
2009

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 96 publications
(42 citation statements)
references
References 38 publications
4
37
1
Order By: Relevance
“…Although glucose generates some InsP3 by Ptdlns4,5P2 hydrolysis the effect is less marked than that of carbachol (27,29,47). Glucose stimulation of Ptdlns4,5P2 hydrolysis appears to depend on the presence of extracellular Ca2+ (7,27,48,49). This Ca>2 dependency is consistent with a Ca2+-mediated activation of phospholipase C (27,50).…”
Section: Discussionmentioning
confidence: 99%
“…Although glucose generates some InsP3 by Ptdlns4,5P2 hydrolysis the effect is less marked than that of carbachol (27,29,47). Glucose stimulation of Ptdlns4,5P2 hydrolysis appears to depend on the presence of extracellular Ca2+ (7,27,48,49). This Ca>2 dependency is consistent with a Ca2+-mediated activation of phospholipase C (27,50).…”
Section: Discussionmentioning
confidence: 99%
“…PLC activity was early detected in rodent islets (Schrey and Montague, 1983;Dunlop and Larkins, 1986), and subsequent analyses have demonstrated islet expression of several PLC-β, -γ, and -δ isozymes Zawalich et al, 1995;Gasa et al, 1999;Zawalich and Zawalich, 2000;Kim et al, 2001a;Kim et al, 2001b). The importance of PLC activity for insulin secretion is underlined by the fact that the enzyme is activated not only after exposure of islets and β-cells to various G-protein coupled receptor stimuli, such as acetylcholine/carbachol (Best and Malaisse, 1983;Hellman and Gylfe, 1986a;Best et al, 1987;Biden et al, 1987;Gilon and Henquin, 2001) and ATP (Gylfe and Hellman, 1987;Blachier and Malaisse, 1988), but also after exposure to glucose (Axen et al, 1983;Best and Malaisse, 1983;Laychock, 1983;Montague et al, 1985) and depolarizing agents (Laychock, 1983;Mathias et al, 1985;Best et al, 1987;Biden et al, 1987;Zawalich and Zawalich, 1988 (Prentki et al, 1988;Gylfe, 1991;Hellman et al, 1992;Theler et al, 1992;Miura et al, 1996) and these oscillations are characterized by a much shorter period than the glucose-induced, slow oscillations described above. Most of the [Ca 2+ ] i -elevating effect is due to IP 3 -mediated Ca 2+ mobilization from the ER, but the emptying of the stores also triggers Ca 2+ entry through store-operated channels in the plasma membrane (Liu and Gylfe, 1997;Miura et al, 1997;Dyachok and Gylfe, 2001).…”
Section: Pip 2 and Signalling Via Phospholipase Cmentioning
confidence: 99%
“…The activation of islet PLC by glucose (Axen et al, 1983;Best and Malaisse, 1983;Laychock, 1983;Montague et al, 1985) and depolarizing agents (Laychock, 1983;Mathias et al, 1985;Best et al, 1987;Biden et al, 1987;Zawalich and Zawalich, 1988) is mainly due to depolarization and Ca 2+ influx, although some glucose-stimulated PIP 2 hydrolysis was reported to proceed even under conditions when elevation of [Ca 2+ ] i was prevented (Best and Malaisse, 1983;Kelley et al, 1995). Real-time imaging studies in isolated insulinoma cells and intact islets (Thore et al, 2004;Tamarina et al, 2005;Thore et al, 2007) have recently confirmed that glucose stimulates PLC activity secondary to the elevation of [Ca 2+ ] i and that membrane depolarization alone (Gromada et al, 1996;Liu et al, 1996) or increase of [Ca 2+ ] i (Mathias et al, 1985;Best et al, 1987;Biden et al, 1987) In addition to contributing to the generation and shaping of Ca 2+ signals, PLC activation can be anticipated to regulate insulin secretion kinetics via generation of DAG and activation of PKC.…”
Section: Pip 2 and Signalling Via Phospholipase Cmentioning
confidence: 99%
“…However, there are different opinions about the mechanisms underlying glucose-induced PLC activation. Whereas several studies indicate that the glucoseinduced phosphoinositide hydrolysis depends on the presence of extracellular Ca 2ϩ (9,11,12), other reports indicate that the process is at least in part Ca 2ϩ independent (13)(14)(15). Recent observations in single insulinoma cells (16) and intact mouse islets (17) have demonstrated that elevation of [Ca 2ϩ ] i is sufficient to trigger PLC activity and that [Ca 2ϩ ] i oscillations are associated with periodic activation of PLC.…”
mentioning
confidence: 99%
“…A large amount of data indicates that PIP 2 plays an important role in the insulin secretory process. It was recognized early that the rate of phosphoinositide metabolism is increased in glucose-stimulated islets (8,9). This effect is due to PLC-mediated hydrolysis of PIP 2 (10).…”
mentioning
confidence: 99%