Regulation of Intracellular Ca2+ Stores by Multiple Ca2+-Releasing Messengers

Cancela, José-Manuel; Petersen, O. H.

doi:10.2337/diabetes.51.2007.s349

Cited by 17 publications

(15 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another important mechanism is the Ca 2+ -induced Ca 2+ release (CICR), by which a depolarizationdependent rise of [Ca 2+ ] i may become amplified by Ca 2+ release from the ER [12]. Even though RyRs are expressed in -cells [13][14][15], the physiological role of cADPr and RyRs remains controversial [16]. Nevertheless, there are several suggestions that RyRs mediate CICR in -cells [12,14,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

“…Due to a high basal Ca 2+ permeability of the ER, SERCA inhibition results in rapid Ca 2+ depletion, but the nature of this leak is not completely understood [16]. In permeabilized cells clamped at Ca 2+ concentrations close to the basal [Ca 2+ ] i levels SERCA inhibition results in release of Ca 2+ from the ER, which is unaffected by inhibitors of IP 3 , ryanodine and NAADP receptors [22,23].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

2004

View full text Add to dashboard Cite

The effect of sarcoendoplasmic reticulum Ca 2+ -ATPase (SERCA) inhibition on the The results indicate that leakage of Ca 2+ from the endoplasmic reticulum after SERCA inhibition is feedback-accelerated by Ca 2+ -induced Ca 2+ release (CICR). In primary pancreatic -cells this CICR is due to activation of inositol 1,4,5-trisphosphate receptors.CICR by ryanodine receptor activation may be restricted to clonal -cells.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

2004

View full text Add to dashboard Cite

show abstract

“…Phosphorylated IRS-1, the product of activated insulin receptor tyrosine kinase (16) (41). In addition to contributing to cytosolic Ca 2ϩ , insulin will change the phosphorylation states of cytosolic proteins; that is, insulin regulates the activity of several Ser/Thr kinases (16).…”

Section: S Srivastava and Hj Gorenmentioning

confidence: 99%

“…Because arginine is able to stimulate first-phase insulin secretion independent of insulin receptors (9), either arginine initiates signaling steps not initiated by glucose or arginine increases intracellular Ca 2ϩ at appropriate sites that can be reproduced by glucose and insulin but not by glucose alone. (41,42). RyR in complex with FK506 binding protein (FKBP12) inhibits Ca 2ϩ exit from intracellular stores.…”

Section: S Srivastava and Hj Gorenmentioning

confidence: 99%

Insulin Constitutively Secreted by β-Cells Is Necessary for Glucose-Stimulated Insulin Secretion

Srivastava

Goren

2003

Diabetes

View full text Add to dashboard Cite

Four hypotheses have been posited on the role of insulin in glucose-stimulated insulin secretion; available evidence has supported insulin as being 1) essential, 2) a positive modulator, 3) a negative modulator, or 4) not necessary. Because circulating insulin levels in mice, before or after intraperitoneal glucose injection, are sufficient to elicit insulin responses in insulinsensitive tissues, it is likely that ␤-cell insulin receptors are continuously exposed to stimulating concentrations of insulin. To determine whether constitutively secreted insulin is necessary for glucose-stimulated insulin secretion, CD1 male mouse islets were incubated for 30 min at 4°C in the absence (control) or presence of anti-insulin (1 g/ml) or anti-IgG (1 g/ml). Then islets were exposed to 3, 11, or 25 mmol/l glucose or to 20 mmol/l arginine. Nontreated islets exhibited first-and second-phase glucose-stimulated insulin secretion. Control and anti-IgG-treated islets, after a 5-min lag phase, increased their insulin secretion in 25 mmol/l glucose. Anti-insulin؊treated islets secreted insulin at a basal rate in 3 or 25 mmol/l glucose buffers. Insulin secretion stimulated by 20 mmol/l arginine was the same in islets pretreated with either antibody and showed no lag phase. Taken together, these data suggest that constitutively secreted insulin is required and sufficient for ␤-cells to maintain sensitivity to glucose.

show abstract

“…3 is the most potent Ca 2ϩ -releasing second messenger that has been shown to regulate many physiological processes, including insulin secretion from pancreatic ␤-cells (1)(2)(3)(4)(5). NAADP induces Ca 2ϩ release through a mechanism distinct from those of other Ca 2ϩ -mobilizing messengers, such as inositol trisphosphate and cyclic ADP-ribose.…”

Section: Nicotinic Acid Adenine Dinucleotide Phosphate (Naadp)mentioning

confidence: 99%

Autocrine/Paracrine Function of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) for Glucose Homeostasis in Pancreatic β-Cells and Adipocytes

Park

Kim

Shawl

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: External application of a Ca 2ϩ -mobilizing messenger, NAADP, to ␤-cells activates intracellular Ca 2ϩ changes and stimulates insulin secretion. Results: NAADP is transported into adipocytes and ␤-cells in a glucose-dependent manner and is also released from pancreatic islets upon stimulation by high glucose. Conclusion: NAADP functions in an auto-/paracrine manner to regulate glucose homeostasis. Significance: NAADP can be exploited as a potential antidiabetic agent.

show abstract

Regulation of Intracellular Ca2+ Stores by Multiple Ca2+-Releasing Messengers

Cited by 17 publications

References 87 publications

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

Insulin Constitutively Secreted by β-Cells Is Necessary for Glucose-Stimulated Insulin Secretion

Autocrine/Paracrine Function of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) for Glucose Homeostasis in Pancreatic β-Cells and Adipocytes

Contact Info

Product

Resources

About