Beta-adrenergic effects on cellular cholesterologenesis and low density lipoprotein metabolism

1991 ◽  
Vol 19 (1) ◽  
pp. 41S-41S
Author(s):  
DAPHNE OWENS ◽  
LUKE O'DONNELL ◽  
PATRICK COLLINS ◽  
ALAN JOHNSON ◽  
GERALD H. TOMKIN
Keyword(s):  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Low Density ◽  
Beta Adrenergic ◽  
Adrenergic Effects

Low density lipoprotein metabolism in rats with puromycin aminonucleoside-induced nephrotic syndrome

Metabolism ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 491-495 ◽  
Author(s):  
J. Joven ◽  
L. Masana ◽  
C. Villabona ◽  
E. Vilella ◽  
T. Bargalló ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Low Density ◽  
Puromycin Aminonucleoside

scholarly journals Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Dietary Fats ◽  
Low Density ◽  
Mrna Levels ◽  
Expression Of Genes ◽  
Coa Reductase

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.

scholarly journals Regulation of low-density-lipoprotein metabolism in the rat

1986 ◽  
Vol 234 (2) ◽  
pp. 493-496 ◽  
Author(s):  
S Bhattacharya ◽  
S Balasubramaniam ◽  
L A Simons
Keyword(s):  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Hormonal Control ◽  
Low Density ◽  
Experimental Conditions ◽  
Synthetic Rate ◽  
Catabolic Rate ◽  
Intermediate Density

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.

Lipid Disorders

2016 ◽  
pp. 179-184
Author(s):  
Ekta Kapoor
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipid Disorders ◽  
Genetic Abnormalities ◽  
Excessive Alcohol

Lipid disorders result from genetic abnormalities in lipoprotein metabolism, other medical conditions (eg, type 2 diabetes mellitus, nephrotic syndrome, hypothyroidism, and excessive alcohol use), and the use of certain drugs (corticosteroids and immunosuppressants The most common disorders in this group are the disorders of low-density lipoprotein cholesterol, which often lead to premature atherosclerosis in patients and their family members.

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