Lipids and atherosclerosis

2004 ◽  
Vol 82 (1) ◽  
pp. 212-224 ◽  
Author(s):  
Patrick C Choy ◽  
Yaw L Siow ◽  
David Mymin ◽  
Karmin O
Keyword(s):  
Plaque Rupture ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cholesterol Absorption ◽  
High Serum ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Liver Uptake ◽  
Receptor System ◽  
High Level

Atherosclerosis is the leading cause of death in North America and within the next two decades will be the leading cause worldwide. Atherosclerosis is characterized by vascular obstruction from the deposits of plaque, resulting in reduced blood flow. Plaque rupture and the consequent thrombosis may lead to sudden blockage of the arteries and cause heart attack. High serum lipid levels, especially the elevated level of low-density lipoprotein (LDL), have been shown to be strongly related to the development of atherosclerosis. It is generally accepted that atherosclerotic lesions are initiated via an enhancement of LDL uptake by monocytes and macrophages. In the liver, uptake of plasma LDL is mediated via specific LDL receptors, but a scavenger receptor system is employed by macrophages. Plasma LDL must be modified prior to uptake by macrophages. Analysis of the lipid content in the oxidatively modified LDL from hyper lipidemic patients revealed that the level of lysophosphatidylcholine was greatly elevated, and the high level of the lysolipid was shown to impair the endothelium-dependent relaxation of the blood vessels. In a separate study, we showed that a high level of homocysteine caused the increase in cholesterol production and apolipoprotein B-100 secretion in hepatic cells. Statins have been used effectively to control the production of cholesterol in the liver, and recently, ezetimibe has been shown to supplement the efficacy of statins by inhibiting cholesterol absorption. The factor of elevated levels of triglyceride-rich lipoproteins in association with depressed high-density lipoproteins, usually in the context of insulin resistance, is an important contributor to atherosclerosis and can be effectively treated with fibric acid derivatives. In hyperhomocysteinemia, folic acid supplements may have a role in the control of cholesterol by reducing the plasma homocysteine level.Key words: atherosclerosis, low density lipoprotein (LDL), homocysteine, statin, folate.

scholarly journals PENGARUH SENAM ZUMBA TERHADAP KADAR TRIGLISERIDA DARAH PADA MAHASISWA FAKULTAS KEDOKTERAN UNIVERSITAS SAM RATULANGI

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Ashael A. Rembang ◽  
J. J. V. Rampengan ◽  
Siantan Supit
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Exercise Session ◽  
Blood Levels ◽  
Normal Body Mass Index ◽  
Low Density ◽  
Research Subjects ◽  
Post Test ◽  
Negative Impacts ◽  
High Level

Abstract: Lipid is classified into several types, which include High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL), Very Low Density Lipoprotein (VLDL) and triglycerides. Triglyceride is a compound consists of three fatty acid molecules esterified into glycerol. Triglycerides are neutral fats synthesized from carbohydrate that are stored in lipid cells. Normal triglyceride levels of human is < 150 mg/dL. High levels of triglyceride have negative impacts on health as it can lead to diseases such as atherosclerosis. High level of triglyceride can be prevented and lowered by exercises such as Zumba exercise. The aim of this study is to know the effect of Zumba exercise on the level of blood triglyceride. This was an experimental study with one group pre-post test design, with criteria that include ages within 16-20 years old, normal Body Mass Index, not a Zumba gymnast, and in healthy condition during research. Samples were 19 female medical faculty students of Sam Ratulangi University class of 2014. They were subjected to do Zumba exercise every day for a week. Triglyceride levels are measured before the first Zumba exercise session and after the final session of Zumba exercise. The data were analyzed using paired-t test with SPSS programme. The results showed that there was a significant change between the mean level of triglyceride before first Zumba exercise 68,11 mg/dL and after Zumba final exercise 48 mg/dL. Conclusion: There was a decrease in triglyceride blood levels of the research subjects after doing Zumba exercises everyday for a week.Keywords: triglyceride, zumba exerciseAbstrak: Lemak terbagi menjadi beberapa jenis, yaitu lemak HDL, lemak LDL, lemak VLDL, serta kadar trigliserida. Trigliserida adalah senyawa yang terdiri dari tiga molekul asam lemak teresterifikasi menjadi gliserol. Trigliserida merupakan lemak netral yang disintesis dari karbohidrat untuk disimpan dalam sel lemak. Kadar trigliserida normal dalam tubuh manusia yaitu <150 mg/dL. Namun kadar trigliserida yang berlebihan juga tidak baik untuk kesehatan. Tingginya kadar trigliserida dalam darah dapat menyebabkan terjadinya penyakit, misalnya aterosklerosis. Kadar trigliserida yang tinggi dapat dicegah dan diturunkan dengan melakukan olahraga seperti senam Zumba. Penelitian ini bertujuan untuk mengetahui pengaruh senam Zumba tehadap kadar trigliserida darah. Penelitian ini bersifat eksperimental dengan rancangan pre-post one group test dengan sampel penelitian yang memenuhi kriteria-kriteria, yaitu usia 16-20 tahun, IMT normal, bukan merupakan seorang atlit atau pesenam Zumba, dan sehat saat dilakukan penelitian. Sampel penelitian adalah mahasiswi Fakultas Kedokteran Universitas Sam Ratulangi angkatan 2014 berjumlah 19 orang. Subjek penelitian melakukan latihan setiap hari dalam seminggu. Kadar trigliserida diukur sebelum latihan Zumba pertama dan sesudah latihan Zumba terakhir. Hasil data dianalisis dengan uji t berpasangan menggunakan program SPSS. Berdasarkan penelitian diperoleh hasil yang menunjukkan perubahan yang signifikan dengan rerata kadar triglierida sebelum senam Zumba 68,11 mg/dL dan rerata sesudah senam Zumba 48,00 mg/dL.Simpulan: Terjadi penurunan kadar tigliserida darah dari subjek penelitian setelah melakukan senam Zumba setiap hari selama seminggu.Kata kunci: trigliserida, senam zumba

The interaction of lipolysis products of very low density lipoprotein with plasma high density lipoprotein (HDL): perfusate HDL with plasma HDL subfractions

1987 ◽  
Vol 65 (3) ◽  
pp. 252-260 ◽  
Author(s):  
S. P. Tam ◽  
W. C. Breckenridge
Keyword(s):  
Particle Size ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Molar Ratio ◽  
High Density Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Hdl Subfractions ◽  
Apo E

The nature of the interaction of high density lipoproteins (HDL), formed during lipolysis of human very low density lipoprotein (VLDL) by perfused rat heart, with subfractions of human plasma HDL was investigated. Perfusate HDL, containing apoliproproteins (apo) E, C-II, and C-III but no apo A-I or A-II, was incubated with a subfraction of HDL (HDL-A) containing apo A-I and A-II, but devoid of apo C-II, C-III, and E. The products of the incubation were resolved by heparin-Sepharose or hydroxylapatite chromatography under conditions which allowed the resolution of the initial HDL-A and perfusate HDL. The fractions were analyzed for apolipoprotein content and lipid composition and assessed for particle size by electron microscopy. Following the incubation, the apo-E-containing lipoproteins were distinct from perfusate HDL since they contained apo A-I as a major component and apo C-II and C-III in reduced proportions. However, the HDL-A fraction contained apo C-II and C-III as major constituents. Associated with these changes in apolipoprotein composition, the apo-E-rich lipoproteins acquired cholesteryl ester from the HDL-A fraction and lost phospholipid to the HDL-A fraction. The HDL-A fraction maintained a low unesterified cholesterol/phospholipid molar ratio (0.23), while the apo-E-containing lipoproteins possessed a high ratio (0.75) characteristic of the perfusate HDL. The particle size of apo-E-containing lipoproteins (138.9 ± 22.5 Å; 1 Å = 0.1 nm) was larger than the initial HDL-A (126.5 ± 17.6 Å) or the new HDL-A-like fraction (120.9 ± 17.4 Å) obtained following incubation with perfusate HDL. It is concluded that incubation of perfusate HDL containing apo E, C-II, and C-III with plasma HDL subfractions results in the acquisition of apo A-I and cholesteryl esters by the apo-E-containing perfusate HDL and the loss of apo C-II, C-III, and phospholipid to the plasma HDL-A fraction. The process does not appear to be due to fusion of the particles, since the apo-E-containing lipoproteins maintain a cholesterol/phospholipid ratio distinct from the HDL-A fraction. The data provide evidence for a potential mechanism for the formation of HDL-E, an apo-E-containing lipoprotein of HDL size and density, through lipolysis of VLDL.

scholarly journals The sites of degradation of rat high-density-lipoprotein apolipoprotein E specifically labelled with O-(4-diazo-3-[125I]iodobenzoyl)sucrose

1985 ◽  
Vol 226 (3) ◽  
pp. 715-721 ◽  
Author(s):  
F M Van't Hooft ◽  
A Van Tol
Keyword(s):  
Serum Proteins ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Serum Lipoproteins ◽  
Rat Serum ◽  
Apo E ◽  
Fasted Rats

O-(4-Diazo-3-[125I]iodobenzoyl)sucrose ([125I]DIBS), a novel labelling compound specifically designed to study the catabolic sites of serum proteins [De Jong, Bouma, & Gruber (1981) Biochem. J. 198, 45-51], was applied to study the tissue sites of degradation of serum lipoproteins. [125I]DIBS-labelled apolipoproteins (apo) E and A-I, added in tracer amounts to rat serum, associate with high-density lipoproteins (HDL) just like conventionally iodinated apo E and A-I. No difference is observed between the serum decays of chromatographically isolated [125I]DIBS-labelled and conventionally iodinated HDL labelled specifically in either apo E or apo A-I. When these specifically labelled HDLs are injected into fasted rats, a substantial [125I]DIBS-dependent 125I accumulation occurs in the kidneys and in the liver. No [125I]DIBS-dependent accumulation is observed in the kidneys after injection of labelled asialofetuin or human low-density lipoprotein. It is concluded that the kidneys and the liver are important sites of catabolism of rat HDL apo E and A-I.

scholarly journals Stimulation of triacylglycerol synthesis in rat adipocytes by plasma very-low-density lipoproteins

1978 ◽  
Vol 176 (1) ◽  
pp. 169-174 ◽  
Author(s):  
P Thomopoulos ◽  
M Berthelier ◽  
D Lagrange ◽  
M J Chapman ◽  
M H Laudat
Keyword(s):  
Fatty Acids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
High Density Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Rat Adipocytes ◽  
Triacylglycerol Synthesis

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.

scholarly journals Association of the Endotoxin Antagonist E5564 with High-Density Lipoproteins In Vitro: Dependence on Low-Density and Triglyceride-Rich Lipoprotein Concentrations

2003 ◽  
Vol 47 (9) ◽  
pp. 2796-2803 ◽  
Author(s):  
Kishor M. Wasan ◽  
Olena Sivak ◽  
Richard A. Cote ◽  
Aaron I. MacInnes ◽  
Kathy D. Boulanger ◽  
...  
Keyword(s):  
Human Plasma ◽  
Human Subjects ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Distribution Profile ◽  
Transfer Activity

ABSTRACT The objective of this study was to determine the distribution profile of the novel endotoxin antagonist E5564 in plasma obtained from fasted human subjects with various lipid concentrations. Radiolabeled E5564 at 1 μM was incubated in fasted plasma from seven human subjects with various total cholesterol (TC) and triglyceride (TG) concentrations for 0.5 to 6 h at 37°C. Following these incubations, plasma samples were separated into their lipoprotein and lipoprotein-deficient fractions by ultracentrifugation and were assayed for E5564 radioactivity. TC, TG, and protein concentrations in each fraction were determined by enzymatic assays. Lipoprotein surface charge within control and phosphatidylinositol-treated plasma and E5564’s influence on cholesteryl ester transfer protein (CETP) transfer activity were also determined. We observed that the majority of E5564 was recovered in the high-density lipoprotein (HDL) fraction. We further observed that incubation in plasma with increased levels of TG-rich lipoprotein (TRL) lipid (TC and TG) concentrations resulted in a significant increase in the percentage of E5564 recovered in the TRL fraction. In further experiments, E5564 was preincubated in human TRL. Then, these mixtures were incubated in hypolipidemic human plasma for 0.5 and 6 h at 37°C. Preincubation of E5564 in purified TRL prior to incubation in human plasma resulted in a significant decrease in the percentage of drug recovered in the HDL fraction and an increase in the percentage of drug recovered in the TRL and low-density lipoprotein fractions. These findings suggest that the majority of the drug binds to HDLs. Preincubation of E5564 in TRL prior to incubation in normolipidemic plasma significantly decreased the percentage of drug recovered in the HDL fraction. Modifications to the lipoprotein negative charge did not alter the E5564 concentration in the HDL fraction. In addition, E5564 does not influence CETP-mediated transfer activity. Information from these studies could be used to help identify the possible components of lipoproteins which influence the interaction of E5564 with specific lipoprotein particles.

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