Effect of Substrate Composition and Concentration on Aortic Cholesterol Ester Hydrolase Activity

Enzyme ◽  
1978 ◽  
Vol 23 (2) ◽  
pp. 135-139 ◽  
Author(s):  
J. Patelski ◽  
A. Pioruńska ◽  
M. Pioruńska-Stolzmann
Author(s):  
Toru Todoroki ◽  
Kojiro Matsumoto ◽  
Kiyoaki Watanabe ◽  
Yukio Tashiro ◽  
Makoto Shimizu ◽  
...  

We confirmed accumulation of glycogen and lipids, particularly cholesterol esters, in the liver of a patient with cholesterol ester storage disease (CESD). Hepatic cholesterol ester concentration was 100-200 times that found in normal livers. Analysis of the fatty acid composition indicated a higher proportion (41%) of cholesterol linoleate (C18-2), a slightly lower proportion (33%) of cholesterol oleate (C18-1) and normal proportions (14%) of cholesterol palmitate (C16-0) in the CESD patient compared with the control. This fatty acid composition of cholesterol esters and the fatty acid composition of other classes of lipids in the patient's liver resembled that of LDL. We also found that acid cholesterol ester hydrolase activity in the CESD liver was reduced to 5% of that in the control liver, while neutral cholesterol ester hydrolase activity remained at the control level. These results suggest that accumulated cholesterol esters were derived mainly from serum LDL and that the accumulation resulted from lack of acid cholesterol ester hydrolase.


1978 ◽  
Vol 19 (7) ◽  
pp. 913-916
Author(s):  
L L Gallo ◽  
R Atasoy ◽  
G V Vahouny ◽  
C R Treadwell

1984 ◽  
Vol 62 (2) ◽  
pp. 244-247
Author(s):  
David L. Severson ◽  
L. Joseph Hayden ◽  
Thea Fletcher

Cholesterol ester hydrolase activity was measured in isolated rat hepatocytes and adipocytes. Administration of triiodothyronine to rats resulted in a specific and selective increase in lysosomal acid (pH 4.5) cholesterol ester hydrolase activity in hepatocytes. Since the majority of lipoprotein degradation occurs in liver parenchymal cells (hepatocytes), the stimulation of liver (hepatocyte) acid cholesterol ester hydrolase activity by triiodothyronine could contribute to the hypocholesterolemie action of thyroid hormones. Treatment of rats with 17α-ethynylestradiol to increase the hepatic degradation of lipoproteins did not change acid cholesterol ester hydrolase activity in liver, indicating that the thyroid hormone induced stimulation of acid cholesterol ester hydrolase activity in hepatocytes is not a secondary effect owing to the increased hepatic catabolism of low density lipoproteins (LDL). In contrast to the results with hepatocytes, hyperthyroidism did not increase acid cholesterol ester hydrolase activity in rat adipocytes.


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