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Retinoic acid modifies lipid metabolism in isolated adult and aged rat cerebellum nuclei
Author(s) -
Gaveglio Virginia Lucía,
Giusto Norma María,
Pasquaré Susana Juana
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.819.1
Subject(s) - monoacylglycerol lipase , diacylglycerol lipase , phosphatidic acid , lipid metabolism , diacylglycerol kinase , biochemistry , neurodegeneration , metabolism , phospholipase a2 , enzyme , phospholipase , cerebellum , phospholipid , chemistry , biology , medicine , endocrinology , endocannabinoid system , receptor , disease , protein kinase c , membrane
Nuclear lipid metabolism gives rise to several lipid second messengers that seem to be involved in the regulation of nuclear structure and gene expression. The purpose of the present research was to study the metabolic pathways involved in the metabolism of phosphatidic acid (PA) and its regulation in isolated nuclei from the central nervous system. This study was also conducted in isolated nuclei from aged animals, thus allowing us to analyze the effects of neurodegeneration processes on PA metabolism as a result of aging. Adult (4 mo) and aged (28 mo) rat cerebellums were homogenized and highly purified nuclei were isolated by sucrose‐density ultracentrifugation. Using radiolabelled substrates we demonstrated lipid phosphate phosphatase, diacylglycerol lipase (DAGL), monoacylglycerol lipase (MAGL), lysophosphatidate phosphohydrolase and phospholipase as well as phospholipase type A activities. We further studied their regulation by retinoic acid (RA) which was observed to decrease DAGL, MAGL and PA‐PLA activities. Significant aged‐related changes in the above‐mentioned enzymatic activities as well as in their regulation by RA were observed. Taken together, our results demonstrate a RA‐regulated PA metabolism in rat cerebellum nuclei which could be involved in neurodegeneration processes. This research was funded by: CONICET, FONCyT, SCyT‐UNS.