1,720,983 research outputs found
Decrease of anandamide ratio between visceral and subcutaneous adipose tissues by dietary EPA and DHA phosphatidylcholine improves metabolic syndrome in obese zucker rats
No full textImpaired cholesterol and DNA synthesis in the mediterranean variant of Glucose-6-Phosphate Dehydrogenase deficiency
No full textHEPATIC GLUCOSE-6-PHOSPHATE DEHYDROGENASE, CHOLESTERO-GENESIS AND SERUM LIPOPROTEINS IN LIVER REGENERATION AFTER PARTIAL HEPATECTOMY
No full textLiver regeneration after partial hepatectomy was used as an experimental model for
studying mammalian cell division and replication. The rate of cell proliferation in this
hyperplastic model was correlated with hepatic de novo synthesis of cholesterol, with the
hexose monophosphate shunt pathway of glucose metabolism, and with serum lipoproteins.
An increase of hepatic cholesterol esters and of incorporation of tritiated water in cholesterol
esters was observed at 24 hr after partial hepatectomy. Partial hepatectomy also resulte
Possible role of P-glycoprotein MDR1 in controlling cancer cell esterification by modulating cholesteryl ester uptake from HDL
No full textCHANGES IN THE LIPOPROTEIN PATTERN IN G-6-PD DEFICIENT CHILDREN DURING HAEMOLYTIC CRISIS
No full textA source of cholesteryl esters (CEs) is essential for an efficient antimicrobial response in lypopolisacharide-activated P388D1 macrophages
No full textInhibition of cholesterol esterification influences cholesterol metabolism and infiammatory response in lipopolysacharide-activated P388D1 macrophages
No full text
Inhibition of cholesterol esterification in the control of leukemia proliferation in vitro
No full textThe results showed a highly significant reduction of proliferation rate in leukemia cells treated with each cholesterol esterification inhibitor. This effect was not caused by cell toxicity, as cell morphology and viability were unaffected at the concentrations of inhibitors used. In addition, it appears that changes in the cholesterol biosynthetic pathway are not responsible for the antiproliferative effect observed, being cholesterol synthesis unaffected in leukemia cells with reduced activity of cholesterol esterification. The inhibition of cell proliferation was associated with a reduction of ACAT and MDR1 mRNA expression and conversely with an up-regulation of p-53 protein expression (p53 not shown). Our results imply that cholesterol esters and MDR1 could play a role in the dynamic processes of lipid transport inside the cells. ACAT inhibitors, by reducing cellular cholesterol esters and MDR1 gene expression and through these pathways the proliferation rate of leukemia cells, may warrant consideration as innovative targeted anticancer agents
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