Calcium‐activated, phospholipid‐dependent protein kinase in rat pancreas islets of langerhans

Tanigawa, Keiichiro; Kuzuya, Hideshi; Imura, Hiroo; Taniguchi, Hiroshi; Baba, Shigeaki; Takai, Yoshimi; Nishizuka, Yasutomi

doi:10.1016/0014-5793(82)80436-5

Cited by 105 publications

(39 citation statements)

References 23 publications

(25 reference statements)

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“…Others have also observed stimulation of insulin release by bradykinin (36), ionophore (37), and other drugs, such as furosemide (38) and tumor-promoting phorbol esters (39), which are felt to activate phospholipase(s). Recently it has been shown that exogenous phospholipase C closely mimics the effects of glucose to selectively increase phosphatidylinositol turnover and to augment insulin release (40), apparently by activating a phospholipid-dependent protein kinase C. Interestingly, this kinase was activated by diacylglycerols containing arachidonate,2 linoleate, or oleate but not those containing stearate. It seems reasonable, therefore, to postulate that arachidonic acid release,2 via its oxygenated metabolite(s), may be a common final pathway by which several membrane-active agents, including glucose, promote genase-dependent endogenous ionophores (55,56 (44,45) and may simply relate in part to their use by the beta cell as fuels or the ability to alter intracellular levels of glucose metabolites (45).…”

Section: Discussionmentioning

confidence: 99%

Lipoxygenase Pathway in Islet Endocrine Cells. OXIDATIVE METABOLISM OF ARACHIDONIC ACID PROMOTES INSULIN RELEASE

Metz¹,

VanRollins²,

Strife³

et al. 1983

J. Clin. Invest.

120

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A B S T R A C T Metabolism of arachidonic acid (AA) via the cyclooxygenase pathway reduces glucose-stimulated insulin release. However, metabolism of AA by the lipoxygenase pathway and the consequent effects on insulin secretion have not been simultaneously assessed in the endocrine islet. Both dispersed endocrine cell-enriched pancreatic cells of the neonatal rat, as well as intact islets of the adult rat, metabolized [3H]AA not only to cyclooxygenase products (prostaglandins E2, F2a, and prostacyclin) but also to the lipoxygenase product 12-hydroxyeicosatetraenoic acid (12-HETE). 12-HETE was identified by coelution with authentic tritiated or unlabeled 12-HETE using four high performance liquid chromatographic systems under eight mobile-phase conditions and its identity was confirmed by gas chromatography/mass spectrometry using selected ion monitoring. The predominant effect of exogenous AA (5 gg/ml) was to stimulate insulin release from pancreatic cells grown in monolayer. This effect was concentration-and time-dependent, and reversible. The effect of AA upon insulin release was potentiated by a cyclooxygenase inhibitor (indomethacin) and was prevented by either of two lipoxygenase inhibitors (5,8,11,14-

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Section: Discussionmentioning

confidence: 99%

Lipoxygenase Pathway in Islet Endocrine Cells. OXIDATIVE METABOLISM OF ARACHIDONIC ACID PROMOTES INSULIN RELEASE

Metz¹,

VanRollins²,

Strife³

et al. 1983

J. Clin. Invest.

120

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“…The expression of PKC in rat pancreatic islets (2) suggests that PKC activation is involved in glucose-induced insulin secretion (3,4), although PKC has also been described to be not involved in glucose-induced insulin secretion in mouse ~-cells (5).…”

Section: Introductionmentioning

confidence: 99%

Glucose‐ and phorbol ester‐induced insulin secretion in human insulinoma cells ‐ Association with protein kinase C activation‐

et al. 1998

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SUMMARY. This study examined the effect of glucose and 12-0-tetradecanoylphorbol-13-acetate (TPA) on insulin secretion in isolated human insulinoma cells. In addition, we analyzed conventional PKCa and [3 activation in the membrane fractions, respectively. Treatment with 5 mM and 20 mM glucose for 5 min and 20 min resulted in 6-7-fold increases in insulin secretion, and treatment with 1 ~tM TPA for 5 min also resulted in 3-fold increases in insulin secretion from the basal level. Immunoblot analysis of membrane fractions showed increases in PKCa and ~ immunoreactivities after treatment with 5 mM, 20 mM glucose and 1 p2VI TPA. Translocations of PKCa after treatment with glucose and TPA were greater than those of PKC~ in membrane fractions. These results suggest that TPA independently provokes insulin secretion v/a PKC activation and that PKCa and I~ activation may be involved in insulin secretion in human insulinoma cells.

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“…Closure of ATP-sensitive K ϩ channels (14) then leads to depolarization of the plasma membrane, influx of Ca 2ϩ through voltage-gated Ca 2ϩ channels (15), and secretory vesicle fusion (16). PKC activity is present in both primary pancreatic islets (17) and derived ␤-cell lines (18,19). Furthermore, conventional (␣, ␤I, ␤II; sensitive to Ca 2ϩ and DAG), novel (␦; sensitive to DAG but not Ca 2ϩ ), and atypical (, ; insensitive to Ca 2ϩ and DAG) PKC isoforms (20 -23) have all been reported in islet cells.…”

mentioning

confidence: 99%

Dynamics of Glucose-induced Membrane Recruitment of Protein Kinase C βII in Living Pancreatic Islet β-Cells

Pinton¹,

Tsuboi²,

Ainscow³

et al. 2002

Journal of Biological Chemistry

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The mechanisms by which glucose may affect protein kinase C (PKC) activity in the pancreatic islet ␤-cell are presently unclear. By developing adenovirally expressed chimeras encoding fusion proteins between green fluorescent protein and conventional (␤II), novel (␦), or atypical () PKCs, we show that glucose selectively alters the subcellular localization of these enzymes dynamically in primary islet and MIN6 ␤-cells.

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Calcium‐activated, phospholipid‐dependent protein kinase in rat pancreas islets of langerhans

Cited by 105 publications

References 23 publications

Lipoxygenase Pathway in Islet Endocrine Cells. OXIDATIVE METABOLISM OF ARACHIDONIC ACID PROMOTES INSULIN RELEASE

Lipoxygenase Pathway in Islet Endocrine Cells. OXIDATIVE METABOLISM OF ARACHIDONIC ACID PROMOTES INSULIN RELEASE

Glucose‐ and phorbol ester‐induced insulin secretion in human insulinoma cells ‐ Association with protein kinase C activation‐

Dynamics of Glucose-induced Membrane Recruitment of Protein Kinase C βII in Living Pancreatic Islet β-Cells

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