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Titolo:
SELECTIVE EFFECT OF A DIET-INDUCED DECREASE IN THE ARACHIDONIC-ACID MEMBRANE PHOSPHOLIPID CONTENT ON IN-VITRO PHOSPHOLIPASE-C AND ADENYLATECYCLASE-MEDIATED PITUITARY-RESPONSE TO ANGIOTENSIN-II
Autore:
ALESSIO MLM; LEGER CL; RASOLONJANAHARY R; WANDSCHEER DE; CLAUSER H; ENJALBERT A; KORDON C;
Indirizzi:
CTR PAUL BROCA,INSERM,U159,UNITE NEUROENDOCRINOL,2TER,RUE DALESIA F-75014 PARIS FRANCE CTR PAUL BROCA,INSERM,U159,UNITE NEUROENDOCRINOL F-75014 PARIS FRANCE UNIV FED PERNAMBUCO,DEPT FISIOL & FARMACOL RECIFE PE BRAZIL INSERM,U58 MONTPELLIER FRANCE
Titolo Testata:
Neuroendocrinology
fascicolo: 4, volume: 60, anno: 1994,
pagine: 400 - 409
SICI:
0028-3835(1994)60:4<400:SEOADD>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; VASOACTIVE INTESTINAL PEPTIDE; INOSITOL PHOSPHATE PRODUCTION; RAT ANTERIOR-PITUITARY; PROLACTIN SECRETION; LACTOTROPH CELLS; RELEASE; HORMONE; DOPAMINE; CALCIUM;
Keywords:
FATTY ACIDS; ARACHIDONIC ACID; PHOSPHOLIPIDS; PHOSPHOLIPASE C; ADENYLATE CYCLASE; ANGIOTENSIN II; GROWTH HORMONE; PROLACTIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
M.L.M. Alessio et al., "SELECTIVE EFFECT OF A DIET-INDUCED DECREASE IN THE ARACHIDONIC-ACID MEMBRANE PHOSPHOLIPID CONTENT ON IN-VITRO PHOSPHOLIPASE-C AND ADENYLATECYCLASE-MEDIATED PITUITARY-RESPONSE TO ANGIOTENSIN-II", Neuroendocrinology, 60(4), 1994, pp. 400-409

Abstract

Young rats were fed on an essential fatty acid (EFA)-deprived diet for 6 weeks after weaning. Their pituitary was removed and adenohypophyseal cells dispersed and maintained in culture. Membrane lipids were analyzed and basal and stimulated levels of hormone secretion were measured after 4-day incubation in a culture medium containing or not 160 mu M arachidonic acid 20:4n-6 (AA) in order to obtain EFA-deficient or EFA-restored pituitary cells, respectively. In EFA-deficient cells membrane phosphoglycerides (PGL) were depleted in AA and adrenic acid 22:4n-6; the deficit was overcome by incubation in the presence of AA. Depletion diversely affected PGL classes. AA was highly depleted in choline phosphoglycerides (ChoPG), only moderately depleted in serine and ethanolamine phosphoglycerides (SerPG and EtnPG) and not depleted at all in inositol phosphoglycerides, suggesting preferential preservationof AA in that class of PGL. Restoration of AA by addition of the fatty acid to the culture medium was complete for ChoPG and EtnPG and onlypartial for SerPG. Depressed levels of AA and adrenic acid in PGL were compensated for by a concomitant increase in 20:3n-9 and 22:3n-9. Growth hormone and prolactin (PRL) secretion was assessed by radioimmunoassay and possible effects of a membrane AA deficit on hormone regulation were tested in cells challenged by either growth hormone-releasinghormone, thyrotropin-releasing hormone, angiotensin II (AII), vasoactive intestinal peptide (VIP) or dopamine. Neither basal nor stimulatedgrowth hormone secretion was different from controls in EFA-deficientcells. PRL modulation by VIP or dopamine was not affected either in EFA-deficient cells. In contrast, the capacity of AII, but not of thyrotropin-releasing hormone, to release PRL was markedly decreased in EFA-deprived cells. It was restored by addition of AA to the incubation medium. Parallel depression AII-induced inositol phosphates and cAMP accumulation was also observed after EFA deficiency. When tested on membranes, the paradoxical inhibition of adenylate cyclase by AII documented by previous observations was reinforced in EFA-deficient membranes. In contrast, binding of AII was not affected by EFA deficiency. It isconcluded that under our experimental conditions EFA deficiency affects selectively coupling of the AII receptor to its effecters without alteration of binding. The effect could involve changes in receptor interactions with coupling proteins.

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Documento generato il 27/01/20 alle ore 16:59:50