Arachidonic acid signaling is involved in the mechanism of imidazoline-induced KATP channel-independent stimulation of insulin secretion

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Arachidonic acid signaling is involved in the mechanism of imidazoline-induced K_ATP channel-independent stimulation of insulin secretion. / Sharoyko, V. V.; Zaitseva, I. I.; Leibiger, B.; Efendić, S.; Berggren, P. O.; Zaitsev, S. V.

In: Cellular and Molecular Life Sciences, Vol. 64, No. 22, 11.2007, p. 2985-2993.

Research output: Contribution to journal › Article › peer-review

Author

Sharoyko, V. V. ; Zaitseva, I. I. ; Leibiger, B. ; Efendić, S. ; Berggren, P. O. ; Zaitsev, S. V. / Arachidonic acid signaling is involved in the mechanism of imidazoline-induced K_ATP channel-independent stimulation of insulin secretion. In: Cellular and Molecular Life Sciences. 2007 ; Vol. 64, No. 22. pp. 2985-2993.

BibTeX

@article{89bdeb5b2bde438e92ce55e54b91699f,

title = "Arachidonic acid signaling is involved in the mechanism of imidazoline-induced KATP channel-independent stimulation of insulin secretion",

abstract = "The mechanism by which the novel, pure glucose-dependent insulinotropic, imidazoline derivative BL11282 promotes insulin secretion in pancreatic islets has been investigated. The roles of KATP channels, α2-adrenoreceptors, the I1-receptor- phosphatidylcholine-specific phospholipase (PC-PLC) pathway and arachidonic acid signaling in BL11282 potentiation of insulin secretion in pancreatic islets were studied. Using SUR1(-/-) deficient mice, the previous notion that the insulinotropic activity of BL11282 is not related to its interaction with KATP channels was confirmed. Insulinotropic activity of BL11282 was not related to its effect on α2-adrenoreceptors, I 1-imidazoline receptors or PC-PLC. BL11282 significantly increased [3H]arachidonic acid production. This effect was abolished in the presence of the iPLA2 inhibitor, bromoenol lactone. The data suggest that potentiation of glucose-induced insulin release by BL11282, which is independent of concomitant changes in cytoplasmic free Ca2+ concentration, involves release of arachidonic acid by iPLA2 and its metabolism to epoxyeicosatrienoic acids through the cytochrome P-450 pathway.",

keywords = "Arachidonic acid, BL11282, Calcium-independent phospholipase A, Cytochrome P-450, Imidazolines, Insulin secretion",

author = "Sharoyko, {V. V.} and Zaitseva, {I. I.} and B. Leibiger and S. Efendi{\'c} and Berggren, {P. O.} and Zaitsev, {S. V.}",

year = "2007",

month = nov,

doi = "10.1007/s00018-007-7308-3",

language = "English",

volume = "64",

pages = "2985--2993",

journal = "Cellular and Molecular Life Sciences",

issn = "1420-682X",

publisher = "Birkh{\"a}user Verlag AG",

number = "22",

}

RIS

TY - JOUR

T1 - Arachidonic acid signaling is involved in the mechanism of imidazoline-induced KATP channel-independent stimulation of insulin secretion

AU - Sharoyko, V. V.

AU - Zaitseva, I. I.

AU - Leibiger, B.

AU - Efendić, S.

AU - Berggren, P. O.

AU - Zaitsev, S. V.

PY - 2007/11

Y1 - 2007/11

N2 - The mechanism by which the novel, pure glucose-dependent insulinotropic, imidazoline derivative BL11282 promotes insulin secretion in pancreatic islets has been investigated. The roles of KATP channels, α2-adrenoreceptors, the I1-receptor- phosphatidylcholine-specific phospholipase (PC-PLC) pathway and arachidonic acid signaling in BL11282 potentiation of insulin secretion in pancreatic islets were studied. Using SUR1(-/-) deficient mice, the previous notion that the insulinotropic activity of BL11282 is not related to its interaction with KATP channels was confirmed. Insulinotropic activity of BL11282 was not related to its effect on α2-adrenoreceptors, I 1-imidazoline receptors or PC-PLC. BL11282 significantly increased [3H]arachidonic acid production. This effect was abolished in the presence of the iPLA2 inhibitor, bromoenol lactone. The data suggest that potentiation of glucose-induced insulin release by BL11282, which is independent of concomitant changes in cytoplasmic free Ca2+ concentration, involves release of arachidonic acid by iPLA2 and its metabolism to epoxyeicosatrienoic acids through the cytochrome P-450 pathway.

AB - The mechanism by which the novel, pure glucose-dependent insulinotropic, imidazoline derivative BL11282 promotes insulin secretion in pancreatic islets has been investigated. The roles of KATP channels, α2-adrenoreceptors, the I1-receptor- phosphatidylcholine-specific phospholipase (PC-PLC) pathway and arachidonic acid signaling in BL11282 potentiation of insulin secretion in pancreatic islets were studied. Using SUR1(-/-) deficient mice, the previous notion that the insulinotropic activity of BL11282 is not related to its interaction with KATP channels was confirmed. Insulinotropic activity of BL11282 was not related to its effect on α2-adrenoreceptors, I 1-imidazoline receptors or PC-PLC. BL11282 significantly increased [3H]arachidonic acid production. This effect was abolished in the presence of the iPLA2 inhibitor, bromoenol lactone. The data suggest that potentiation of glucose-induced insulin release by BL11282, which is independent of concomitant changes in cytoplasmic free Ca2+ concentration, involves release of arachidonic acid by iPLA2 and its metabolism to epoxyeicosatrienoic acids through the cytochrome P-450 pathway.

KW - Arachidonic acid

KW - BL11282

KW - Calcium-independent phospholipase A

KW - Cytochrome P-450

KW - Imidazolines

KW - Insulin secretion

UR - http://www.scopus.com/inward/record.url?scp=38549122935&partnerID=8YFLogxK

U2 - 10.1007/s00018-007-7308-3

DO - 10.1007/s00018-007-7308-3

M3 - Article

C2 - 17922229

VL - 64

SP - 2985

EP - 2993

JO - Cellular and Molecular Life Sciences

JF - Cellular and Molecular Life Sciences

SN - 1420-682X

IS - 22

ER -

ID: 5533006