scholarly journals Effect of 25-hydroxycholesterol and bile acids on the regulation of cholesterol metabolism in Hep G2 cells

1989 ◽  
Vol 264 (1) ◽  
pp. 241-247 ◽  
Author(s):  
T L Carlson ◽  
B A Kottke
Keyword(s):  
Acetic Acid ◽  
Bile Acids ◽  
Cholesterol Synthesis ◽  
Cholesterol Metabolism ◽  
Mrna Levels ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Control Value ◽  
Apo E ◽  
G2 Cells

The effect of 25-hydroxycholesterol (25-OH-cholesterol) and chenodeoxycholic (CDC) acid on apoprotein secretion, low-density lipoprotein receptor activity, and [3H]triacylglycerol secretion in Hep G2 cells was studied. Both 25-OH-cholesterol and CDC acid increased the secretion of apolipoprotein (apo) E by Hep G2 cells. The secretion of apo A-I was slightly lowered (less than 10% disease). The maximal increase in apo E secretion was observed in culture medium containing 2 micrograms of 25-OH-cholesterol/ml or 10 micrograms of CDC acid/ml plus 10% fetal calf serum. Cholesterol, 7-OH-cholesterol and other bile acids were ineffective in inducing increases in apo E secretion. Another cholesterol synthesis inhibitor, mevinolin, was also ineffective in generating an increase in apoprotein secretion. The data indicated a specific interaction between 25-OH-cholesterol or CDC acid and apo E secretion in Hep G2 cells. Cholesterol synthesis, as measured by the incorporation of [14C]acetic acid into sterols, was repressed in Hep G2 cells in the presence of 25-OH-cholesterol (17% of control value). CDC acid, on the other hand, increased [14C]acetic acid incorporation (156% of control value). The number of LDL receptors in Hep G2 cells was decreased after incubation with 25-OH-cholesterol (62% of control value), but increased significantly after incubation with CDC acid (149% of control value). The secretion of [3H]triacylglycerol by Hep G2 cells incubated with 25-OH-cholesterol was greatly increased (248% of control value). On the contrary, CDC acid did not cause any increase in [3H]triacylglycerol secretion. The above results suggest that 25-OH-cholesterol and CDC acid have different effects on lipid metabolism in Hep G2 cells. The mRNA levels of apo E increased in cells preincubated with 25-OH-cholesterol and CDC acid, which suggested that the increase in apo E secretion is at least partly due to an increase in synthesis.

Synthesis of bile acids in Hep G2 cells: effect of substrate supply

1987 ◽  
Vol 15 (3) ◽  
pp. 411-412
Author(s):  
EMELYN R. ELDREDGE ◽  
KATHLEEN M. BOTHAM ◽  
C. ROLAND WOLF ◽  
KEITH E. SUCKLING
Keyword(s):  
Bile Acids ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Substrate Supply ◽  
G2 Cells

Effect of ketoconazole on cholesterol synthesis and on HMG-COA reductase and LDL-receptor activities in Hep G2 cells

1987 ◽  
Vol 36 (8) ◽  
pp. 1245-1249 ◽  
Author(s):  
Herman Jan Kempen ◽  
Kees Van Son ◽  
Louis H. Cohen ◽  
Marieke Griffioen ◽  
Hans Verboom ◽  
...  
Keyword(s):  
Cholesterol Synthesis ◽  
Ldl Receptor ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

scholarly journals Cholesterol and bile acid synthesis in Hep G2 cells. Metabolic effects of 26- and 7 α-hydroxycholesterol

1989 ◽  
Vol 262 (3) ◽  
pp. 989-992 ◽  
Author(s):  
N B Javitt ◽  
K Budai
Keyword(s):  
Chenodeoxycholic Acid ◽  
Cholesterol Synthesis ◽  
Lithocholic Acid ◽  
Biological Effects ◽  
Acid Synthesis ◽  
Bile Acid Synthesis ◽  
Metabolic Effects ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells

1. Using a human hepatoma (Hep G2) cell line that continually synthesizes 3 beta-hydroxy-5-cholenoic acid, lithocholic acid, chenodeoxycholic acid and cholic acid we have determined the metabolism and biological effects of 26-hydroxycholesterol and 7 alpha-hydroxycholesterol. 2. Addition of 26-hydroxycholesterol to the medium (6 microM) downregulated cholesterol and chenodeoxycholic acid synthesis. 3. The predominant metabolite of 26-hydroxycholesterol was 3 beta-hydroxy-5-cholenoic acid. 4. Cholesterol synthesis was not affected by the addition of 7 alpha-hydroxycholesterol (6 and 12 microM). The predominant metabolite of 7 alpha-hydroxycholesterol was chenodeoxycholic acid. 5. In Hep G2 cells 7 alpha-hydroxylation of 26-hydroxycholesterol is not well expressed.

The Production of Heparin Cofactor li Is Not Regulated by Inflammatory Cytokines in Human Hepatoma Cells: Comparison with Plasminogen Activator Inhibitor Type-1

1996 ◽  
Vol 75 (02) ◽  
pp. 298-302 ◽  
Author(s):  
Chisato Kolke ◽  
Yumiko Hayakawa ◽  
Kenji Niiya ◽  
Nobuo Sakuragawa ◽  
Hideo Sasaki
Keyword(s):  
Plasminogen Activator Inhibitor ◽  
Mrna Levels ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Tnf Α ◽  
G2 Cells ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor

SummaryUsing the Northern blot technique, we screened 6 human hepatoma cell lines to investigate the regulation mechanism of heparin cofactor II (HCII) biosynthesis. We found that HuH-7 and Hep G2 cells constitutively expressed the HC II gene. In conditioned medium, HuH-7 cells constantly produced HC II that was functionally active and formed a complex with thrombin in the presence of dermatan sulfate. HC II is thought be an acute phase reactant, and, therefore, we examined the effects of the major inflammatory cytokines, IL-6, IL-1β, and TNF-α, on the regulation of HC II production in HuH-7 and Hep G2 cells. In HuH-7 cells, the antigen and mRNA levels of plasminogen activator inhibitor type-1 (PAI-1), an acute phase protein produced by hepa-tocytes, were increased in response to stimulation with either IL-6 or IL-1 (3 or both, but HC II antigen and mRNA levels were not changed by the same stimulation. Even when Hep G2 cells were treated with a combination of three cytokines, IL-6, IL-1β, and TNF-α, HC II antigen and mRNA levels were not changed; however, PAI-1 antigen and mRNA levels were clearly increased. These results suggest that the production of HC II in hepatoma cells is not regulated by the major inflammatory mediators, IL-6, IL-iβ, and TNF-α.

Effect of ethanol on cell growth and cholesterol metabolism in cultured Hep G2 cells

2003 ◽  
Vol 81 (6) ◽  
pp. 379-386 ◽  
Author(s):  
Mónica P Polo ◽  
Margarita G de Bravo ◽  
María JT de Alaniz
Keyword(s):  
Growth Rate ◽  
Cell Growth ◽  
Culture Medium ◽  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

The Hep G2 human hepatoma cell line has been recognized as an excellent in vitro human model system. For this reason, this line was used to study the effect of ethanol on HMG-CoA reductase activity concerning cell growth and cholesterol metabolism. Cells were incubated in ethanol-containing medium (0–400 mmol/L) for up to 102 h. Ethanol caused an inhibition in the growth rate and in HMG-CoA reductase activity that could be reverted by the removal of ethanol from the culture medium, indicating no cellular damage. These changes cannot be ascribed to the regulatory effect of cholesterol levels, since its content was not modified either in the cells or in the medium. The addition of mevalonate to the culture medium could not revert the growth rate inhibition evoked by ethanol. Moreover, ethanol produced an increment in the cholesterol efflux in [3H]cholesterol-prelabeled cells. We conclude that the decrease in HMG-CoA reductase activity evoked by ethanol treatment on Hep G2 cells would not be the cause but the consequence of the impairment in cellular growth, since this impairment could not be reverted by the addition of mevalonate to the culture medium.Key words: ethanol, cholesterol, HMG-CoA reductase, hepatoma cells, lipid metabolism.

scholarly journals Effect of a novel squalene epoxidase inhibitor, NB-598, on the regulation of cholesterol metabolism in Hep G2 cells

1991 ◽  
Vol 266 (20) ◽  
pp. 13171-13177
Author(s):  
Y. Hidaka ◽  
H. Hotta ◽  
Y. Nagata ◽  
Y. Iwasawa ◽  
M. Horie ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Squalene Epoxidase ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells
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