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hepatoblastoma/triacylglycerol
Länken sparas på Urklipp
5 resultat
Niacin accelerates intracellular ApoB degradation by inhibiting triacylglycerol synthesis in human hepatoblastoma (HepG2) cells.
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The mechanism by which the potent drug niacin decreases apoB-containing atherogenic lipoproteins and prevents coronary disease is unclear. Utilizing human hepatoblastoma (HepG2) cells as an in vitro model, we have examined the effect of niacin on intracellular degradation of apoB and the regulatory
Inhibitory effect of gastrin peptides on triacylglycerol secretion in Hep G2 cells.
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OBJECTIVE
To determine whether human liver cells respond to gastrin peptides by reducing their secretion of triacylglycerols, as recently observed in rat hepatocytes.
METHODS
Cells of the human hepatoblastoma cell line Hep G2 were incubated with pentagastrin and heptadeca gastrin, followed by lipid
Interaction of non-esterified fatty acid and insulin in control of triacylglycerol secretion by Hep G2 cells.
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The role of insulin in the regulation of plasma triacylglycerol is poorly understood. Conflicting actions of insulin on rat liver cells have been reported, insulin inhibiting triacylglycerol secretion in short incubations (less than 24 h) and stimulating triacylglycerol secretion in longer
Control of Hep G2-cell triacylglycerol and apolipoprotein B synthesis and secretion by polyunsaturated non-esterified fatty acids and insulin.
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Non-esterified fatty acids (NEFAs) and insulin are important factors in the control of lipoprotein secretion, but the mechanism of action is unclear. The present study was undertaken to determine whether insulin and NEFAs modulated hepatic secretion of triacylglycerol and apolipoprotein B (apo-B) by
Hepatic farnesyl diphosphate synthase expression is suppressed by polyunsaturated fatty acids.
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Dietary vegetable oils and fish oils rich in PUFA (polyunsaturated fatty acids) exert hypocholesterolaemic and hypotriglyceridaemic effects in rodents. The plasma cholesterol-lowering properties of PUFA are due partly to a diminution of cholesterol synthesis and of the activity of the rate-limiting
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