scholarly journals Dietary cholesterol reduces lipoprotein lipase activity in the atherosclerosis-susceptible Bio F1B hamster

2003 ◽  
Vol 89 (3) ◽  
pp. 341-350 ◽  
Author(s):  
Martina A. McAteer ◽  
David C. Grimsditch ◽  
Martin Vidgeon-Hart ◽  
G. Martin Benson ◽  
Andrew M. Salter
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Plasma Cholesterol ◽  
Dietary Cholesterol ◽  
Lipoprotein Metabolism ◽  
Coconut Oil ◽  
Hdl Cholesterol ◽  
High Cholesterol Diet ◽  
Lipoprotein Lipase Activity ◽  
Golden Syrian Hamster

We have compared lipoprotein metabolism in, and susceptibility to atherosclerosis of, two strains of male Golden Syrian hamster, the Bio F1B hybrid and the dominant spot normal inbred (DSNI) strain. When fed a normal low-fat diet containing approximately 40 g fat and 0·3 g cholestero/g, triacylglycerol-rich lipoprotein (chylomicron+VLDL) and HDL-cholesterol were significantly higher (P<0·001) in Bio F1B hamsters than DSNI hamsters. When this diet was supplemented with 150 g coconut oil and either 0·5 or 5·0 g cholestero/g, significant differences were seen in response. In particular, the high-cholesterol diet produced significantly greater increases in plasma cholesterol and triacylglycerol in the Bio F1B compared with the DSNI animals (P=0·002 and P<0·001 for cholesterol and triacylglycerol, respectively). This was particularly dramatic in non-fasting animals, suggesting an accumulation of chylomicrons. In a second experiment, animals were fed 150 g coconut oi/g and 5·0 g cholestero/g for 6 and 12 months. Again, the Bio F1B animals showed dramatic increases in plasma cholesterol and triacylglycerol, and this was confirmed as primarily due to a rise in chylomicron concentration. Post-heparin lipoprotein lipase activity was significantly reduced (P<0·001) in the Bio F1B compared with the DSNI animals at 6 months, and virtually absent at 12 months. Bio F1B animals were also shown to develop significantly more (P<0·001) atherosclerosis. These results indicate that, in the Bio F1B hybrid hamster, cholesterol feeding reduces lipoprotein lipase activity, thereby causing the accumulation of chylomicrons that may be associated with their increased susceptibility to atherosclerosis.

scholarly journals Changes in lipoprotein lipase activity and plasma liver lipids in thiram intoxicated rats.

1993 ◽  
Vol 40 (4) ◽  
pp. 563-567 ◽  
Author(s):  
B Sadurska ◽  
B Boguszewski
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Plasma Cholesterol ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Plasma Lipoproteins ◽  
Total Plasma Cholesterol ◽  
Total Plasma ◽  
Lipoprotein Lipase Activity ◽  
Liver Lipids

Acute thiram (tetramethyl-bis-thiocarbamyl disulphide) poisoning of rat (a single dose of 50% LD50) caused decreased lipoprotein lipase (LPL) activity in adipose tissue, the greatest inhibition being observed at 72 h after administration of the pesticide. Simultaneously, the levels of total plasma cholesterol, triacylglycerols and the high density lipoprotein (HDL) cholesterol were increased. On repeated pesticide administration (5% LD50) decreased LPL activity was observed after 14 and 30 days of poisoning, whereas after 90 days the LPL activity was distinctly increased. The levels of total cholesterol (in all periods of poisoning) and HDL cholesterol (only after 30 days of poisoning) became increased. These changes were accompanied by decreased content of free fatty acids and increase of hepatic triacylglycerols. The changes observed in the lipoprotein lipase activity of thiram-poisoned rats correspond to the profiles of plasma lipoproteins typical of thyroid hypofunction.

Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8

2021 ◽  
Author(s):  
Kelli L. Sylvers-Davie ◽  
Brandon S.J. Davies
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Lipoprotein Metabolism ◽  
Fatty Acid Uptake ◽  
Extracellular Proteins ◽  
Current Understanding ◽  
Acid Uptake ◽  
Lipoprotein Lipase Activity

Triglyceride-rich lipoproteins deliver fatty acids to tissues for oxidation and for storage. Release of fatty acids from circulating lipoprotein triglycerides is carried out by lipoprotein lipase (LPL), thus LPL serves as a critical gatekeeper of fatty acid uptake into tissues. LPL activity is regulated by a number of extracellular proteins including three members of the angiopoietin-like family of proteins. In this review we discuss our current understanding of how, where, and when ANGPTL3, ANGPTL4, and ANGPTL8 regulate lipoprotein lipase activity, with a particular emphasis on how these proteins interact with each other to coordinate triglyceride metabolism and fat partitioning.

High muscle lipoprotein lipase activity in thyrotoxic patients

1985 ◽  
Vol 109 (2) ◽  
pp. 227-231 ◽  
Author(s):  
H. Lithell ◽  
B. Vessby ◽  
I. Selinus ◽  
P. A. Dahlberg
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Elimination Rate ◽  
Lipoprotein Metabolism ◽  
Tolerance Test ◽  
Serum Lipoprotein ◽  
Cholesterol Concentration ◽  
High Density Lipoproteins ◽  
Lipoprotein Lipase Activity ◽  
Enhanced Sensitivity

Abstract. Serum lipoprotein metabolism was studied in 7 women before and after treatment for thyrotoxicosis. Of the lipoprotein lipids, the triglyceride concentration in the low density lipoproteins (LDL) (P < 0.01) and the cholesterol concentration in both LDL (P < 0.01) and the high density lipoproteins (HDL) (P < 0.05) increased significantly during treatment. These changes were accompanied by increases in apolipoprotein B (P < 0.01) and A-1 (P < 0.05) concentrations in serum. Muscle lipoprotein lipase activity (LPLA) was increased in the thyrotoxic state by 46% (P < 0.05) compared with the value after the patients had been rendered euthyroid, but adipose tissue LPLA was only 8% higher (ns) in the former state. The capacity for removal of exogenous fat, as determined by the fractional elimination rate (K2) at an iv fat tolerance test, was 23% higher in the thyrotoxic than in the euthyroid state (ns). It is suggested that the increase in muscle LPLA in the thyrotoxic state may be due to enhanced sensitivity to catecholamines. This may contribute to the increased capacity for plasma triglyceride turnover in thyrotoxicosis.

Effect of Triton on Lipoprotein Lipase of Rat Plasma

1957 ◽  
Vol 188 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Michael C. Schotz ◽  
A. Scanu ◽  
Irvine H. Page
Keyword(s):  
Fatty Acids ◽  
Lipoprotein Lipase ◽  
Intravenous Injection ◽  
Optical Density ◽  
Lipase Activity ◽  
Coconut Oil ◽  
Rat Plasma ◽  
Plasma Lipoproteins ◽  
Lipoprotein Lipase Activity ◽  
Oil Emulsion

When postheparin plasma was incubated with a coconut oil substrate, a decrease in optical density and an increase in unesterified fatty acids occurred. The increase in unesterified acids was prevented by previous intravenous injection of Triton to rats. Addition of post-Triton plasma to a system containing postheparin plasma and coconut oil emulsion inhibited the lipoprotein lipase activity. Incubation of Triton with coconut oil substrate before addition of postheparin plasma caused inhibition of lipoprotein lipase activity. It is concluded that inhibition of lipoprotein lipase activity by Triton is due to modification of the substrate such that the enzyme can no longer act. Further, it is suggested that the chief cause of Triton hyperlipemia is coating of the plasma lipoproteins by Triton resulting in their faulty catabolism.

Dietary coconut oil affects more lipoprotein lipase activity than the mitochondria oxidative capacities in muscles of preruminant calves

2000 ◽  
Vol 11 (4) ◽  
pp. 231-238 ◽  
Author(s):  
Cécile Piot ◽  
Jean-François Hocquette ◽  
Patrick Herpin ◽  
Jacques H Veerkamp ◽  
Dominique Bauchart
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Coconut Oil ◽  
Lipoprotein Lipase Activity
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