scholarly journals Possible Inhibitory Effect of Lipid Peroxides on Acid Lipase Activity via Low-Density Lipoprotein in Human Mononuclear Leukocytes.

1991 ◽  
Vol 11 (2) ◽  
pp. 129-138 ◽  
Author(s):  
Fusako MAEHIRA ◽  
Ikuko MIYAGI ◽  
Shinzoh KOHNO ◽  
Fukuichi NAKADA
Keyword(s):  
Lipase Activity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Peroxides ◽  
Inhibitory Effect ◽  
Mononuclear Leukocytes ◽  
Low Density ◽  
Acid Lipase ◽  
Human Mononuclear Leukocytes

scholarly journals Decreased sensitivity of very-low-density lipoprotein secretion to the inhibitory effect of insulin in cultured hepatocytes from lactating rats

1996 ◽  
Vol 316 (3) ◽  
pp. 737-741 ◽  
Author(s):  
Catherine S. BOURGEOIS ◽  
Geoffrey F. GIBBONS
Keyword(s):  
Milk Fat ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Defined Medium ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Inhibitory Effects ◽  
Insulin Resistant ◽  
Lactating Mammary Gland

Hepatocytes were prepared from 10–11-day lactating rat dams and from lactating dams which had been weaned for periods of either 1–2 days or 7 days. Hepatocytes from each group were cultured for periods of up to 48 h in a chemically defined medium. Compared with those from the 7-day weaned animals, hepatocytes from the lactating rats were resistant to the inhibitory effects of insulin on the secretion of very-low-density lipoprotein (VLDL) triacylglycerol (TAG). These differences persisted for up to 48 h in culture. Hepatocytes from the 1–2-day weaned animals remained relatively insulin-resistant in this respect. Similar differences in the response to insulin were not observed for the secretion of VLDL apolipoprotein B. TAG production increased and ketogenesis decreased in the hepatocytes from the lactating compared with those from the 7-day weaned rats. Insensitivity of the liver to the normal effects of insulin on the secretion of VLDL TAG may arise from a need to maintain an adequate flux of hepatic lipids to the lactating mammary gland in order to meet the large demand for milk-fat production.

scholarly journals Morphological characterization of the cholesteryl ester cycle in cultured mouse macrophage foam cells.

1983 ◽  
Vol 97 (4) ◽  
pp. 1156-1168 ◽  
Author(s):  
D J McGookey ◽  
R G Anderson
Keyword(s):  
Cholesteryl Ester ◽  
Lipase Activity ◽  
Lipid Droplets ◽  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
The Body ◽  
Cyclic Process ◽  
Low Density ◽  
Cholesteryl Esters

Mouse peritoneal macrophages can be induced to accumulate cholesteryl esters by incubating them in the presence of acetylated low density lipoprotein. The cholesteryl esters are sequestered in neutral lipid droplets that remain in the cell even when the acetylated low density lipoprotein is removed from the culture media. Previous biochemical studies have determined that the cholesterol component of cholesteryl ester droplets constantly turns over with a half time of 24 h by a cyclic process of de-esterification and re-esterification. We have used morphologic techniques to determine the spatial relationship of cholesteryl ester, free cholesterol, and lipase activity during normal turnover and when turnover is disrupted. Lipid droplets were surrounded by numerous 7.5-10.0-nm filaments; moreover, at focal sites on the margin of each droplet there were whorles of concentrically arranged membrane that penetrated the matrix. Histochemically detectable lipase activity was associated with these stacks of membrane. Using filipin as a light and electron microscopic probe for free cholesterol, we determined that a pool of free cholesterol was associated with each lipid droplet. Following incubation in the presence of the exogenous cholesterol acceptor, high density lipoprotein, the cholesteryl ester droplets disappeared and were replaced with lipid droplets of a different lipid composition. Inhibition of cholesterol esterification caused cholesteryl ester droplets to disappear and free cholesterol to accumulate in numerous myelin-like structures in the body of the cell.

scholarly journals Regulation of very-low-density-lipoprotein lipid secretion in hepatocyte cultures derived from diabetic animals

1989 ◽  
Vol 262 (1) ◽  
pp. 313-319 ◽  
Author(s):  
J M Duerden ◽  
S M Bartlett ◽  
G F Gibbons
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Whole Body ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Short Period ◽  
Streptozotocin Diabetic Rats ◽  
Cholesterol Secretion

Hepatocytes were derived from 2-3-day streptozotocin-diabetic rats and maintained in culture for up to 3 days. Compared with similar cultures from normal animals, these hepatocytes secreted less very-low-density-lipoprotein (VLDL) triacylglycerol, but the decrease in the secretion of VLDL non-esterified and esterified cholesterol was not so pronounced. This resulted in the secretion of relatively cholesterol-rich VLDL particles by the diabetic hepatocytes. Addition of insulin for a relatively short period (24 h) further decreased the low rates of VLDL triacylglycerol secretion from the diabetic hepatocytes. The secretion of VLDL esterified and non-esterified cholesterol also declined. These changes occurred irrespective of whether or not exogenous fatty acids were present in the culture medium. Little or no inhibitory effect of insulin was observed after longer-term (24-48 h) exposure to the hormone. Both dexamethasone and a mixture of lipogenic precursors (lactate plus pyruvate) stimulated VLDL triacylglycerol and cholesterol secretion, but not to the levels observed in hepatocytes from normal animals. The low rate of hepatic VLDL secretion in diabetes contrasts with the increase in whole-body VLDL production rate. This suggests that the intestine is a major source of plasma VLDL in insulin-deficient diabetes.

scholarly journals Chronic exogenous hyperinsulinaemia does not modify the acute inhibitory effect of insulin on the secretion of very-low-density lipoprotein triacylglycerol and apolipoprotein B in primary cultures of rat hepatocytes

1996 ◽  
Vol 314 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Catherine S. BOURGEOIS ◽  
David WIGGINS ◽  
Geoffrey F. GIBBONS
Keyword(s):  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Primary Cultures ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Cell Protein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Plasma Insulin Concentration

Male Wistar rats were fitted with subcutaneous osmotic minipumps that delivered insulin at a constant rate of 0.20 i.u./h for 7 days. This treatment raised the plasma insulin concentration from 31±4 to 201±64 μ-i.u./ml. Hepatocytes prepared from the hyperinsulinaemic animals secreted very-low-density lipoprotein (VLDL) triacylglycerol (TAG) at a higher rate (172±21 μg per 24 h per mg cell protein) than did those from sham-operated controls (109±12 μg per 24 h per mg) (P < 0.05). However, chronic exogenous hyperinsulinaemia had no stimulatory effect on the secretion of VLDL apolipoprotein B (apoB) in derived hepatocytes compared with those from the sham-operated controls (2.32±0.38 compared with 3.09±0.40 μg per 24 h per mg). Hepatocytes from the hyperinsulinaemic rats thus secreted larger VLDL particles as evidenced by the increased TAG:apoB ratio (78.4±13.1 compared with 38.4±7.6; P < 0.05). In hepatocytes from the hyperinsulinaemic rats a larger proportion of the newly synthesized TAG was secreted as VLDL. Hepatocytes from the hyperinsulinaemic and the sham-operated control animals were equally sensitive to the inhibitory effect of insulin added in vitro on the secretion of VLDL TAG. Insulin added in vitro to the culture medium of hepatocytes from hyperinsulinaemic animals significantly decreased the TAG:apoB ratio of the secreted VLDL. This change did not occur in hepatocytes from sham-operated rats. These results suggest that, in vivo, chronic hyperinsulinaemia is not in itself sufficient to desensitize the liver to the acute inhibitory effect of insulin on the secretion of VLDL.

Determinative Role of Peroxidized Low-Density Lipoprotein in Myocardial Thromboxane Synthesis during Pacing-Induced Ischaemia in Humans

1998 ◽  
Vol 94 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Hsiu-Ching Hsu ◽  
Ming-Fong Chen ◽  
Chii-Ming Lee ◽  
Yuan-Teh Lee
Keyword(s):  
Coronary Sinus ◽  
Low Density Lipoprotein ◽  
Lactate Production ◽  
Density Lipoprotein ◽  
Thromboxane A2 ◽  
Lipid Peroxides ◽  
Atrial Pacing ◽  
Low Density ◽  
Blood Samples ◽  
Coronary Sinus Blood

1. Myocardial thromboxane A2 production increases in patients with pacing-induced ischaemia and correlates with a decrease in myocardial lactate extraction. The release of myocardial thromboxane A2 before any lactate production was observed in patients with unstable angina. This study was proposed to clarify whether the early thromboxane A2 release contributed to the ongoing myocardial ischaemia and to determine which metabolites can be attributed to the thromboxane A2 release. Thirty-five patients with chest pain and positive treadmill exercise test underwent atrial pacing to the predicted maximal heart rate. The pacing was maintained at this peak rate for 10 min, then ceased. Blood samples of the ascending aorta and coronary sinus were drawn simultaneously at rest, at 2 and 10 min of peak-pacing, and 5 and 10 min after termination of the pacing; samples were used for analyses of lipid profiles, prostacyclin, thromboxane A2, lactate and lipid peroxides on plasma and low-density lipoprotein particles. 2. Twenty out of 35 patients who displayed pacing-induced ischaemia were documented by electrocardiographic evidence of ST depression >2 mm developing after 2 min of peak-pacing [ischaemic group, STΔ(+)]. They had (i) negative fractional lactate extraction; (ii) pacing-induced decreases of plasma thromboxane A2 levels in the coronary sinus blood (564 ± 57 versus 479 ± 47 ng/l, P < 0.05) at 2 min of peak-pacing; the data increased at 10 min of peak-pacing (564 ± 57 versus 620 ± 60 ng/l, P < 0.05), then returned to baseline levels at 5 and 10 min post-pacing; (iii) significantly increased lipid peroxides on low-density lipoprotein of the coronary sinus blood at 2 and 10 min of peak-pacing (each P < 0.001), as well as at 5 min post-pacing (P < 0.05); (iv) significant correlation between thromboxane A2 levels and lipid peroxides on low-density lipoprotein of the coronary sinus blood samples. 3. In STΔ(+) patients, myocardial thromboxane synthesis changed before lactate production and correlated with the increase of lipid peroxides on low-density lipoprotein of the coronary venous blood. This implies that lipid peroxides on low-density lipoprotein participate in thromboxane production and play a determinative role in pacing-induced ischaemia.

scholarly journals The role of high-density lipoprotein and lipid-soluble antioxidant vitamins in inhibiting low-density lipoprotein oxidation

1993 ◽  
Vol 294 (3) ◽  
pp. 829-834 ◽  
Author(s):  
M I Mackness ◽  
C Abbott ◽  
S Arrol ◽  
P N Durrington
Keyword(s):  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Antioxidant Vitamins ◽  
Ldl Oxidation ◽  
Low Density ◽  
Conjugated Diene ◽  
Peroxide Formation

1. The oxidation of low-density lipoprotein (LDL) is believed to play a central role in atherogenesis. We have compared the effect of antioxidant vitamins and high-density lipoprotein (HDL) on the Cu(2+)-catalysed oxidation of LDL. 2. Antioxidant vitamin supplementation significantly reduced conjugated diene formation but did not affect the formation of lipid peroxides. 3. Conversely, HDL did not affect conjugated diene formation but inhibited the formation of lipid peroxides by up to 90%. 4. The inhibition by HDL of lipid peroxide formation in oxidized LDL was dependent on the concentration of HDL and was not due to HDL chelating Cu2+. 5. Large interindividual variations in the inhibition of lipid peroxide formation by autologous HDL were evident, which were related to the rate of lipid peroxide generation in the LDL. 6. We conclude that HDL is a powerful antioxidant or more probably inhibitor of LDL oxidation in vitro and may play an important role in vivo in preventing atherosclerosis by inhibiting LDL oxidation in the artery wall.

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