Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein B-100

1995 ◽  
Vol 89 (s33) ◽  
pp. 15P-16P
Author(s):  
MH Cummings ◽  
GF Watts ◽  
R Naoumova ◽  
AM Umpleby ◽  
JM Kelly ◽  
...  
Keyword(s):  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Secretion Rate ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Substrate Availability

Increased hepatic secretion of very-low-density lipoprotein apolipoprotein B-100 in cholesteryl ester storage disease

1995 ◽  
Vol 41 (1) ◽  
pp. 111-114 ◽  
Author(s):  
M H Cummings ◽  
G F Watts
Keyword(s):  
Cholesteryl Ester ◽  
Apolipoprotein B ◽  
Storage Disease ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mevalonic Acid ◽  
Secretion Rate ◽  
Gas Chromatography Mass Spectrometry ◽  
Very Low Density Lipoprotein ◽  
Low Density

Abstract Using a stable isotope method, we measured the hepatic secretion rate of very-low-density lipoprotein apolipoprotein B-100 (VLDL apoB) in a 26-year-old women who had dyslipidemia due to cholesteryl ester storage disease (CESD) and in five normolipidemic subjects. [1-13C]Leucine was administered by a primed constant intravenous infusion and the enrichment of VLDL apoB was determined by gas chromatography-mass spectrometry. The absolute secretion rate (ASR) of VLDL apoB in the patient was more than twice the mean ASR of the normolipidemic group (17.1 vs 8.0 +/- 0.8 mg/kg body wt. per day). The plasma mevalonic acid concentration, a measure of intrahepatic cholesterol synthesis, was also greater in the patient than in the normolipidemic subjects (8.3 vs 4.4 +/- 1.8 micrograms/L). The findings are consistent with the hypothesis that in CESD increased intrahepatic synthesis of cholesterol stimulates hepatic secretion of VLDL apoB and this may partly account for the dyslipidemia.

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