scholarly journals Triglyceride is Significantly Increased in Remnant Lipoproteins After Food Intake and its Association with Lipoprotein Lipase in the Plasma

2018 ◽  
pp. 6-10
Author(s):  
Katsuyuki Nakajima ◽  
Yoshiharu Tokita ◽  
Akira Tanaka
Keyword(s):  
Insulin Resistance ◽  
Food Intake ◽  
Lipoprotein Lipase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Meal Intake ◽  
Remnant Lipoproteins ◽  
Key Word ◽  
Definitive Role

This article introduces the characteristics of postprandial Very Low Density Lipoprotein (VLDL) remnants (remnant lipoproteins; RLP) in plasma which significantly increased after fat load as a major component of increased Triglycerides (TG) and involved in obesity and insulin resistance. It has been long believed that postprandial RLP, mainly Chylomicron (CM) remnants, increases as the result of disturbed lipoprotein lipase (LPL) activity caused by insulin resistance, etc. However, based on this report, we recently proposed that elevated postprandial VLDL remnants produced by food intake, such as excessive fat and fructose, cause obesity and insulin resistance when exposed continuously [1]. VLDL remnants, but not CM remnants, is the key word of this article and VLDL remnants play a definitive role as a “bridge” between food intake and its metabolism. Here, we have explained the bridging role of VLDL remnants between the habit of food intake and its metabolism in body. Following 6 aspects between fat-rich meal intake and the increase of plasma postprandial TG and RLP are explained. (1) Why TG and RLP increase after food intake? (2) Which lipoproteins increase most after food intake? (3) What percentage of increased TG after food is comprised of RLP-TG? (4) How the increased TG is metabolized by LPL? (5) The increase of postprandial RLP is the result of obesity and insulin resistance or cause of obesity and insulin resistance? (6)Why postprandial TG is a risk of cardiovascular diseases?

The role of lipoprotein lipase in metabolism of normolipidemic very low density lipoprotein by macrophages

1989 ◽  
Vol 9 (1) ◽  
pp. 48-52
Author(s):  
Shi-Fing Wang ◽  
You-mei Feng ◽  
Zong-chen Feng ◽  
Wan-sheng Wu ◽  
Chun-ben Wang ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

Removal of triacylglycerols from chylomicrons and VLDL by capillary beds: the basis of lipoprotein remnant formation

2007 ◽  
Vol 35 (3) ◽  
pp. 472-476 ◽  
Author(s):  
F. Karpe ◽  
A.S. Bickerton ◽  
L. Hodson ◽  
B.A. Fielding ◽  
G.D. Tan ◽  
...  
Keyword(s):  
Stable Isotopes ◽  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Lipase Activity ◽  
Remnant Lipoproteins ◽  
Triacylglycerol Content

The triacylglycerol content of chylomicrons and VLDL (very-low-density lipoprotein) compete for the same lipolytic pathway in the capillary beds. Although chylomicron triacylglycerols appear to be the favoured substrate for lipoprotein lipase, VLDL particles compete in numbers. Methods to quantify the specific triacylglycerol removal from VLDL and chylomicrons may involve endogenous labelling of the triacylglycerol substrate with stable isotopes in combination with arteriovenous blood sampling in humans. Arteriovenous quantification of remnant lipoproteins suggests that adipose tissue with its high lipoprotein lipase activity is a principal site for generation of remnant lipoproteins. Under circumstances of reduced efficiency in the removal of triacylglycerols from lipoproteins, there is accumulation of remnant lipoproteins, which are potentially atherogenic.

scholarly journals The Importance of Lipoprotein Lipase Regulation in Atherosclerosis

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 782
Author(s):  
Anni Kumari ◽  
Kristian K. Kristensen ◽  
Michael Ploug ◽  
Anne-Marie Lund Winther
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Lipoprotein Lipase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Atherosclerotic Cardiovascular Disease ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Remnant Lipoproteins ◽  
Atherosclerosis Development

Lipoprotein lipase (LPL) plays a major role in the lipid homeostasis mainly by mediating the intravascular lipolysis of triglyceride rich lipoproteins. Impaired LPL activity leads to the accumulation of chylomicrons and very low-density lipoproteins (VLDL) in plasma, resulting in hypertriglyceridemia. While low-density lipoprotein cholesterol (LDL-C) is recognized as a primary risk factor for atherosclerosis, hypertriglyceridemia has been shown to be an independent risk factor for cardiovascular disease (CVD) and a residual risk factor in Atherosclerosis development. In this review, we focus on the lipolysis machinery and discuss the potential role of triglycerides, remnant particles, and lipolysis mediators in the onset and progression of Atherosclerotic cardiovascular disease (ASCVD). This review details a number of important factors involved in the maturation and transportation of LPL to the capillaries, where the triglycerides are hydrolyzed, generating remnant lipoproteins. Moreover, LPL and other factors involved in intravascular lipolysis are also reported to impact the clearance of remnant lipoproteins from plasma and promote lipoprotein retention in capillaries. Apolipoproteins (Apo) and angiopoietin-like proteins (ANGPTLs) play a crucial role in regulating LPL activity and recent insights into LPL regulation may elucidate new pharmacological means to address the challenge of hypertriglyceridemia in Atherosclerosis development.

The Role of the Low-Density Lipoprotein Receptor-Related Protein (LRP) in the Plasma Clearance and Liver Uptake of Recombinant Single-chain Urokinase-type Plasminogen Activator in Rats

1997 ◽  
Vol 77 (04) ◽  
pp. 710-717 ◽  
Author(s):  
Marieke E van der Kaaden ◽  
Dingeman C Rijken ◽  
J Kar Kruijt ◽  
Theo J C van Berkel ◽  
Johan Kuiper
Keyword(s):  
Plasminogen Activator ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Single Chain ◽  
Liver Uptake ◽  
Type Plasminogen Activator ◽  
Parenchymal Liver ◽  
Urokinase Type Plasminogen Activator ◽  
Density Lipoprotein Receptor

SummaryUrokinase-type plasminogen activator (u-PA) is used as a thrombolytic agent in the treatment of acute myocardial infarction. In vitro, recombinant single-chain u-PA (rscu-PA) expressed in E.coli is recognized by the Low-Density Lipoprotein Receptor-related Protein (LRP) on rat parenchymal liver cells. In this study we investigated the role of LRP in the liver uptake and plasma clearance of rscu-PA in rats. A preinjection of the LRP inhibitor GST-RAP reduced the maximal liver uptake of 125I-rscu-PA at 5 min after injection from 50 to 30% of the injected dose and decreased the clearance of rscu-PA from 2.37 ml/min to 1.58 ml/min. Parenchymal, Kupffer and endothelial cells were responsible for 40, 50 and 10% of the liver uptake, respectively. The reduction in liver uptake of rscu-PA by the preinjection of GST-RAP was caused by a 91 % and 62% reduction in the uptake by parenchymal and Kupffer cells, respectively. In order to investigate the part of rscu-PA that accounted for the interaction with LRP, experiments were performed with a mutant of rscu-PA lacking residues 11-135 (= deltal25- rscu-PA). Deletion of residues 11-135 resulted in a 80% reduction in liver uptake and a 2.4 times slower clearance (0.97 ml/min). The parenchymal, Kupffer and endothelial cells were responsible for respectively 60, 33 and 7% of the liver uptake of 125I-deltal25-rscu-PA. Preinjection of GST-RAP completely reduced the liver uptake of delta 125-rscu-PA and reduced its clearance to 0.79 ml/min. Treatment of isolated Kupffer cells with PI-PLC reduced the binding of rscu-PA by 40%, suggesting the involvement of the urokinase-type Plasminogen Activator Receptor (u-PAR) in the recognition of rscu-PA. Our results demonstrate that in vivo LRP is responsible for more than 90% of the parenchymal liver cell mediated uptake of rscu-PA and for 60% of the Kupffer cell interaction. It is also suggested that u-PAR is involved in the Kupffer cell recognition of rscu-PA.

The Role of the Endothelium in Premature Atherosclerosis: Molecular Mechanisms

2020 ◽  
Vol 27 (7) ◽  
pp. 1041-1051 ◽  
Author(s):  
Michael Spartalis ◽  
Eleftherios Spartalis ◽  
Antonios Athanasiou ◽  
Stavroula A. Paschou ◽  
Christos Kontogiannis ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Low Density Lipoprotein ◽  
Critical Role ◽  
Density Lipoprotein ◽  
Number Of Genes ◽  
Causes Of Mortality ◽  
Artery Disease ◽  
Genetic And Environmental Factors ◽  
Made In

Atherosclerotic disease is still one of the leading causes of mortality. Atherosclerosis is a complex progressive and systematic artery disease that involves the intima of the large and middle artery vessels. The inflammation has a key role in the pathophysiological process of the disease and the infiltration of the intima from monocytes, macrophages and T-lymphocytes combined with endothelial dysfunction and accumulated oxidized low-density lipoprotein (LDL) are the main findings of atherogenesis. The development of atherosclerosis involves multiple genetic and environmental factors. Although a large number of genes, genetic polymorphisms, and susceptible loci have been identified in chromosomal regions associated with atherosclerosis, it is the epigenetic process that regulates the chromosomal organization and genetic expression that plays a critical role in the pathogenesis of atherosclerosis. Despite the positive progress made in understanding the pathogenesis of atherosclerosis, the knowledge about the disease remains scarce.

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