Low density lipoprotein metabolism in Type IV and Type V hyperlipoproteinemia

Metabolism ◽  
1979 ◽  
Vol 28 (1) ◽  
pp. 4-8 ◽  
Author(s):  
Jacob G. Brook ◽  
Harald Torsvik ◽  
Robert S. Lees ◽  
Martha A. McCluskey ◽  
Henry A. Feldman
1992 ◽  
Vol 20 (3) ◽  
pp. 197-210 ◽  
Author(s):  
H H Ditschuneit ◽  
M Flechtner-Mors ◽  
E Hagel ◽  
H Ditschuneit

After an oral fat load of 1 g/kg body weight in 10 obese females with hyperlipoproteinaemia type IV, serum triglycerides concentrations were maximal at 4 h with a slight decline at 6 h, whereas serum cholesterol concentrations rose slightly at 4 h and 6 h. After 6 h, concentrations of triglycerides and cholesterol were significantly increased in chylomicrons and very low-density lipoprotein (VLDL), whereas cholesterol concentrations were decreased in high-density lipoprotein 2 (HDL2) plus HDL3. After oral treatment with 450 mg gemfibrozil twice daily for 28 days, triglyceride concentrations were reduced in serum, chylomicrons, VLDL and low-density lipoprotein, and total cholesterol concentrations were reduced in serum, chylomicrons and VLDL, and increased in HDL2 plus HDL3. At 6 h after a fat load following 28 days' gemfibrozil treatment, triglyceride and cholesterol concentrations were reduced in serum, chylomicrons and VLDL when compared with pretreatment results. It is concluded that gemfibrozil is effective in lowering triglycerides and cholesterol, particularly in triglyceriderich particles, and raising the cholesterol content of HDL2 plus HDL3. After an oral fat load gemfibrozil inhibits the increase in serum cholesterol and partly prevents postprandial hypertriglyceridaemia.


Metabolism ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 491-495 ◽  
Author(s):  
J. Joven ◽  
L. Masana ◽  
C. Villabona ◽  
E. Vilella ◽  
T. Bargalló ◽  
...  

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.


1986 ◽  
Vol 234 (2) ◽  
pp. 493-496 ◽  
Author(s):  
S Bhattacharya ◽  
S Balasubramaniam ◽  
L A Simons

The mechanism of regulation of plasma low-density-lipoprotein (LDL) metabolism in the rat was studied under a number of experimental conditions. LDL clearance and uptake in the liver was measured after intravenous pulse injection of [14C]sucrose-labelled LDL alone or in combination with reductively methylated [3H]sucrose-labelled LDL. Hyperthyroid rats showed a significant increase in fractional catabolic rate (FCR) and the proportion of LDL degraded in the liver, whereas the synthetic rate of LDL increased by 50%. Receptor-mediated clearance increased 2-fold. Hypothyroid rats showed a significant increase in LDL concentration. The FCR and proportion of LDL degraded in the liver were decreased significantly. Receptor-mediated clearance was also reduced. Cholesterol feeding increased chylomicron, very-low-density-and intermediate-density-lipoprotein cholesterol concentrations, but there was no change in the LDL concentration, FCR or the synthetic rate of LDL. Cholestyramine feeding did not induce changes in the kinetic parameters. These results indicate that, in the rat, the hepatic LDL-receptor pathway is under hormonal control, whereas cholesterol and cholestyramine feeding have no demonstrated effect on LDL metabolism.


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