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Artículo

Insulin Action on Polyunsaturated Phosphatidic Acid Formation in Rat Brain: An “In Vitro” Model with Synaptic Endings from Cerebral Cortex and Hippocampus

Zulian, Sandra EdithIcon ; Ilincheta, Monica GracielaIcon ; Giusto, Norma MariaIcon
Fecha de publicación: 12/2009
Editorial: Springer/Plenum Publishers
Revista: Neurochemical Research
ISSN: 0364-3190
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Otras Ciencias Biológicas

Resumen

The highly efficient formation of phosphatidic acid from exogenous 1-stearoyl-2-arachidonoyl-sn-glycerol (SAG) in rat brain synaptic nerve endings (synaptosomes) from cerebral cortex and hippocampus is reported. Phosphatidic acid synthesized from SAG or 1,2-dipalmitoylsn-glycerol (DPG) was 17.5 or 2.5 times higher, respectively, than from endogenous synaptosomal diacylglycerides. Insulin increased diacylglycerol kinase (DAGK) action on endogenous substrate in synaptic terminals from hippocampus and cerebral cortex by 199 and 97%, respectively. Insulin preferentially increased SAG phosphorylation from hippocampal membranes. In CC synaptosomes insulin increased phosphatidic acid (PA) synthesis from SAG by 100% with respect to controls. Genistein (a tyrosine kinase inhibitor) inhibited this stimulatory insulin effect. Okadaic acid or cyclosporine, used as Ser/Threo protein phosphatase inhibitors, failed to increase insulin effect on PA formation. GTPcS and particularly NaF were potent stimulators of PA formation from polyunsaturated diacylglycerol but failed to increase this phosphorylation when added after 5 min of insulin exposure. GTPcS and NaF increased phosphatidylinositol 4,5 bisphosphate (PIP2) labeling with respect to controls when SAG was present. On the contrary, they decreased polyphosphoinositide labeling with respect to controls in the presence of DPG. Our results indicate that a DAGK type 3 (DAGKe) which preferentially, but not selectively, utilizes 1-acyl-2-arachidonoyl-sn-glycerol and which could be associated with polyphosphoinositide resynthesis, participates in synaptic insulin signaling. GTPcS and NaF appear to be G protein activators related to insulin and the insulin receptor, both affecting the signaling mechanism that augments phosphatidic acid formation.
Palabras clave: Synaptosomes , Insulin , Phosphatidic Acid , Diacylglycerol
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
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URI: http://hdl.handle.net/11336/41676
URL: https://link.springer.com/article/10.1007%2Fs11064-008-9901-8
DOI: http://dx.doi.org/10.1007/s11064-008-9901-8
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Articulos de INST.DE INVEST.BIOQUIMICAS BAHIA BLANCA (I)
Citación
Zulian, Sandra Edith; Ilincheta, Monica Graciela; Giusto, Norma Maria; Insulin Action on Polyunsaturated Phosphatidic Acid Formation in Rat Brain: An “In Vitro” Model with Synaptic Endings from Cerebral Cortex and Hippocampus; Springer/Plenum Publishers; Neurochemical Research; 34; 7; 12-2009; 1236-1248
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