triacylglycerol/crise epiléptica

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Cerebral phosphoinositide, triacylglycerol and energy metabolism during sustained seizures induced by bicuculline.

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In ventilated rats, levels of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), diacylglycerol (DAG), triacylglycerol (TAG), free fatty acids (FFA) and phosphatidic acid, as well as their fatty acid contents, were measured in forebrain

Effect of various drugs producing convulsive seizures on rat brain glycerolipid metabolism.

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Convulsive seizures were elicited in the rat by the injection of several different drugs (pyridoxal phosphate, bicuculline, penicillin and ouabain). Glycerolipid metabolism was studied after the intraventricular injection of [2-3H]glycerol, which was incorporated into rat brain glycerides. The

Reduced labeling of brain phosphatidylinositol, triacylglycerols, and diacylglycerols by [1-14C]arachidonic acid after electroconvulsive shock: potentiation of the effect by adrenergic drugs and comparison with palmitic acid labeling.

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The effect of electroconvulsive shock on the labeling of phospholipids and neutral lipids in mice brains was examined after intracerebral injection of [1-14C] arachidonic acid or [1-14C]palmitic acid. Electroconvulsive shock reduced greatly the removal of radiolabeled arachidonic acid from the free

Metabolic, Reproductive, and Neurologic Abnormalities in Agpat1-Null Mice.

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Defects in the biosynthesis of phospholipids and neutral lipids are associated with cell membrane dysfunction, disrupted energy metabolism, and diseases including lipodystrophy. In these pathways, the 1-acylglycerol-3-phosphate O-acyltransferase (AGPAT) enzymes transfer a fatty acid to the sn-2

Neutral lipid storage with acid lipase deficiency: a new variant of Wolman's disease with features of the Senior syndrome.

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A girl presented with small stature, obesity, tapetoretinal degeneration, deafness, psychomotor regression, seizures, acanthosis nigricans, hepatomegaly, and chronic tubulointerstitial nephropathy. She died at age ten with renal insufficiency and uncontrolled seizures. Histochemistry showed lipid

Mechanism of depression of brain phospholipid levels by an epileptogenic drug.

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Treatment of the rat with U18666A [3 beta-(2-diethylaminoethoxy) androst-5-en-17-one HCl] resulted in development of a chronic seizure state and 20-40% reductions in the concentration of all major phospholipid in whole brain. The mechanism of the phospholipid changes was explored in the present

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