scholarly journals An Overview on Hyperlipidemia

2021 ◽  
pp. 543-555
Author(s):  
D. A. Helen Sheeba ◽  
R. Gandhimathi
Keyword(s):  
Plasma Lipids ◽  
Medical Condition ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Research Work ◽  
Density Lipoprotein ◽  
High Plasma ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density

Introduction: Hyperlipidemia is a medical condition indicated by an increase in one or more plasma lipids, such as triglycerides, cholesterol, cholesterol esters, phospholipids, and/or plasma lipoproteins, such as very low-density lipoprotein and low-density lipoprotein, as well as decreased levels of high-density lipoprotein. This increase in plasma lipids is one of the most important risk factors for cardiovascular disease. In the meanwhile, statins and fibrates remain the most common anti-hyperlipidemic drugs for treating high plasma cholesterol and triglycerides. Conclusion: Hence this review focused to study of hyperlipidemia. This review is useful to research work in hyperlididemia.

scholarly journals A Global Review Article on Hyperlipidemia

2021 ◽  
Vol 68 (1) ◽  
Author(s):  
Mumthaj. P ◽  
Natarajan. P ◽  
Janani. A.M ◽  
Vijay. J ◽  
Gokul. V
Keyword(s):  
Plasma Lipids ◽  
Medical Condition ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Review Article ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Factors Associated

Hyperlipidemia is a medical condition characterized by an increase in one or more of the plasma lipids, including triglycerides, cholesterol, cholesterol esters, phospholipids and or plasma lipoproteins including very low-density lipoprotein and low-density lipoprotein along with reduced high-density lipoprotein levels. This elevation of plasma lipids is among the leading risk factors associated with cardiovascular diseases. Introduction, type of lipoprotein, classification of hyperlipidemia, Complications of hyperlipidaemia, causes; Symptoms of hypelipedemia, Pathogenesis of hyperlipidemia, Pathogenesis of hyperlipidemia, diagnosis, prevention, treatments.

Plasma Lipid and Lipoprotein Abnormalities in Patients with Malabsorption

1973 ◽  
Vol 45 (5) ◽  
pp. 583-592 ◽  
Author(s):  
Gilbert R. Thompson ◽  
J. Paul Miller
Keyword(s):  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Serum Triglyceride ◽  
Plasma Lipoproteins ◽  
Low Density ◽  
Cholesterol Levels ◽  
Lipids And Lipoproteins

1. Plasma lipids and lipoproteins have been studied in control subjects and patients with various types of steatorrhoea. 2. Low plasma cholesterol levels were found in malabsorbers and were associated with decreased amounts of low-density lipoprotein (LDL) in males and high-density lipoprotein (HDL) in females. 3. Serum triglyceride levels were normal in males, but exceeded control values in some of the females, due to an increase in very-low-density lipoprotein. 4. LDL composition was abnormal in both male and female malabsorbers, with a decreased proportion of cholesterol ester and an increased proportion of triglyceride. There was also an increased proportion of triglyceride in HDL. 5. These findings show that malabsorption markedly influences not only the concentration but also the composition of plasma lipoproteins.

Effects of dietary protein on composition and turnover of apoproteins in plasma lipoproteins of rabbits

1981 ◽  
Vol 59 (8) ◽  
pp. 642-647 ◽  
Author(s):  
D. C. K. Roberts ◽  
M. E. Stalmach ◽  
M. W. Khalil ◽  
J. C. Hutchinson ◽  
K. K. Carroll
Keyword(s):  
Soy Protein ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Dietary Proteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Isolated Soy Protein ◽  
Intermediate Density

The hypercholesterolemia and atherosclerosis produced in rabbits by feeding cholesterol-free, semipurified diets are due to the use of casein as the protein component of such diets and can be prevented by replacing the casein with isolated soy protein. To investigate the reasons for the differing effects of these dietary proteins on plasma cholesterol levels, plasma lipoproteins were isolated from rabbits fed semipurified diets containing either casein or isolated soy protein, labeled with 125I, and reinjected into rabbits fed one or other of these two diets. 125I-labeled apoproteins of intermediate density lipoprotein, isolated from rabbits on either diet, turned over more rapidly in rabbits fed soy protein compared with those fed casein. 125I-labeled apoproteins of very low density lipoprotein from rabbits fed soy protein were transferred to high density lipoprotein more rapidly than those from rabbits fed casein. In this case, the results were determined primarily by the diet fed to the donor rabbits, but the diet fed to the recipients also appeared to have some influence. The apoproteins of plasma lipoproteins from rabbits fed casein or soy protein were separated by isoelectric focussing and tentatively identified by comparison of their isoelectric points with those of apoproteins from human plasma lipoproteins. The concentration of apoprotein E was markedly increased in the very low density and intermediate density lipoproteins of casein-fed rabbits, and apoprotein C was also increased in the very low density lipoprotein of rabbits fed casein, compared with those fed soy protein. Effects of dietary proteins on plasma cholesterol may be secondary to their effects on the composition and metabolism of the protein components of plasma lipoproteins.

Studies on the Thromboplastic Effect of Human Plasma Lipoproteins

1976 ◽  
Vol 35 (01) ◽  
pp. 178-185 ◽  
Author(s):  
Helena Sandberg ◽  
Lars-Olov Andersson
Keyword(s):  
High Density Lipoprotein ◽  
Human Plasma ◽  
Platelet Rich Plasma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Free Plasma ◽  
Good Agreement

SummaryHuman plasma lipoprotein fractions were prepared by flotation in the ultracentrifuge. Addition of these fractions to platelet-rich, platelet-poor and platelet-free plasma affected the partial thromboplastin and Stypven clotting times to various degrees. Addition of high density lipoprotein (HDL) to platelet-poor and platelet-free plasma shortened both the partial thromboplastin and the Stypven time, whereas addition of low density lipoprotein and very low density lipoprotein (LDL + VLDL) fractions only shortened the Stypven time. The additions had little or no effect in platelet-rich plasma.Experiments involving the addition of anti-HDL antibodies to plasmas with different platelet contents and measuring of clotting times produced results that were in good agreement with those noted when lipoprotein was added. The relation between structure and the clot-promoting activity of various phospholipid components is discussed.

The Passage of Apoproteins from Plasma Lipoproteins into the Lipoproteins of Peripheral Lymph in Man

1977 ◽  
Vol 53 (3) ◽  
pp. 221-226
Author(s):  
D. Reichl ◽  
N. B. Myant ◽  
J. J. Pflug ◽  
D. N. Rudra
Keyword(s):  
Intravenous Injection ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Intermediate Density Lipoprotein ◽  
Peripheral Lymph ◽  
Apoprotein B ◽  
Intermediate Density

1. The transport of apoprotein B from the lipoproteins of plasma into the lipoproteins of lymph draining the foot has been studied in four men with type III hyperlipoproteinaemia. 2. Three subjects were given autologous 125I-labelled very-low-density lipoprotein (VLDL) and 131I-labelled low-density lipoprotein (LDL) by intravenous injection; the fourth was given autologous 125I-labelled VLDL and 131I-labelled intermediate-density lipoprotein (IDL) plus LDL. 3. The 125I/131I ratios in serum and lymph apoprotein B, and the 125I and 131I specific radioactivities of apoprotein B in VLDL, IDL and LDL from serum and lymph, indicate that apoprotein B in the circulating VLDL can reach peripheral lymph without the intermediacy of circulating LDL.

scholarly journals (Pro)renin Receptor Inhibition Reduces Plasma Cholesterol and Triglycerides but Does Not Attenuate Atherosclerosis in Atherosclerotic Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Dien Ye ◽  
Xiaofei Yang ◽  
Liwei Ren ◽  
Hong S. Lu ◽  
Yuan Sun ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Inflammatory Responses ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Low Density ◽  
Beneficial Effects ◽  
Receptor Inhibition ◽  
Density Lipoprotein Receptor

Objective: Elevated plasma cholesterol concentrations contributes to ischemic cardiovascular diseases. Recently, we showed that inhibiting hepatic (pro)renin receptor [(P)RR] attenuated diet-induced hypercholesterolemia and hypertriglyceridemia in low-density lipoprotein receptor (LDLR) deficient mice. The purpose of this study was to determine whether inhibiting hepatic (P)RR could attenuate atherosclerosis.Approach and Results: Eight-week-old male LDLR−/− mice were injected with either saline or N-acetylgalactosamine-modified antisense oligonucleotides (G-ASOs) primarily targeting hepatic (P)RR and were fed a western-type diet (WTD) for 16 weeks. (P)RR G-ASOs markedly reduced plasma cholesterol concentrations from 2,211 ± 146 to 1,128 ± 121 mg/dL. Fast protein liquid chromatography (FPLC) analyses revealed that cholesterol in very low-density lipoprotein (VLDL) and intermediate density lipoprotein (IDL)/LDL fraction were potently reduced by (P)RR G-ASOs. Moreover, (P)RR G-ASOs reduced plasma triglyceride concentrations by more than 80%. Strikingly, despite marked reduction in plasma lipid concentrations, atherosclerosis was not reduced but rather increased in these mice. Further testing in ApoE−/− mice confirmed that (P)RR G-ASOs reduced plasma lipid concentrations but not atherosclerosis. Transcriptomic analysis of the aortas revealed that (P)RR G-ASOs induced the expression of the genes involved in immune responses and inflammation. Further investigation revealed that (P)RR G-ASOs also inhibited (P)RR in macrophages and in enhanced inflammatory responses to exogenous stimuli. Moreover, deleting the (P)RR in macrophages resulted in accelerated atherosclerosis in WTD fed ApoE−/− mice.Conclusion: (P)RR G-ASOs reduced the plasma lipids in atherosclerotic mice due to hepatic (P)RR deficiency. However, augmented pro-inflammatory responses in macrophages due to (P)RR downregulation counteracted the beneficial effects of lowered plasma lipid concentrations on atherosclerosis. Our study demonstrated that hepatic (P)RR and macrophage (P)RR played a counteracting role in atherosclerosis.

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