Plasma Lipid Variability in the Toronto Twin Register

1980 ◽  
Vol 29 (4) ◽  
pp. 299-302 ◽  
Author(s):  
Jean Milner ◽  
Joe C. Christian ◽  
David Hewitt
Keyword(s):  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Total Plasma Cholesterol ◽  
Total Plasma ◽  
Low Density Lipoprotein Cholesterol ◽  
Mz Twins

Plasma lipids were studied on 92 pairs of twins (66 MZ and 26 like-sexed DZ). The DZ twins had significantly greater total variance than the MZ twins for total plasma cholesterol but not for triglycerides or the high, low, and very low-density lipoprotein cholesterol fractions.

Effect of Phenobarbitone on Plasma Lipids in Normal Subjects

1976 ◽  
Vol 50 (5) ◽  
pp. 349-353 ◽  
Author(s):  
P. N. Durrington ◽  
C. J. C. Roberts ◽  
Lyn Jackson ◽  
R. A. Branch ◽  
M. Hartog
Keyword(s):  
Ldl Cholesterol ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Normal Subjects ◽  
Low Density ◽  
Total Plasma Cholesterol ◽  
Total Plasma ◽  
Antipyrine Clearance

1. Phenobarbitone in a dose of 180 mg daily was administered to ten normal subjects for 3 weeks. There was a significant increase in total plasma cholesterol, plasma low-density-lipoprotein cholesterol, plasma low-density-lipoprotein (LDL) triglycerides and plasma LDL protein. The increase in plasma LDL cholesterol accounted for the increase in total plasma cholesterol. There was a significant reduction in the ratio of LDL cholesterol to LDL protein. 2. No significant changes were observed in total plasma triglycerides, plasma very-low-density-lipoprotein (VLDL) triglycerides, plasma VLDL cholesterol or plasma VLDL protein. 3. Evidence that drug-metabolizing enzymes were induced by phenobarbitone was provided by an increase in antipyrine clearance. No relationship was observed between changes in plasma cholesterol and changes in antipyrine clearance. Serum γ-glutamyl transpeptidase was also increased after phenobarbitone administration, the increase being unrelated to changes in antipyrine clearance or plasma cholesterol.

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.

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.

Lipoprotein Profiles in a Family with Two Mutants of Apolipoprotein E: Possible Association with Hypertriglyceridaemia but Not with Dysbetalipoproteinaemia

1994 ◽  
Vol 86 (3) ◽  
pp. 323-329 ◽  
Author(s):  
Shui-Ping Zhao ◽  
Arn M. J. M. Van den Maagdenberg ◽  
Ton F. F. P. Vroom ◽  
Ferdinand M. Van't Hooft ◽  
Jan A. Gevers Leuven ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Family Members ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Molar Ratio ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Profiles

1. The plasma lipoprotein profiles of eight members of a Dutch pedigree spanning three generations where two rare apolipoprotein E mutants, APOE*3(Cys-112→Arg; Arg-251→Gly) and APOE*2(Val-236 →Glu), segregate were analysed to determine whether the APOE mutants were associated with dyslipidaemia. 2. The proband, a 51-year-old Caucasian male, was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly) and his spouse was a carrier of APOE*2(Val-236→Glu). Four other family members were carriers of one or both of the mutant APOE genes. 3. The plasma cholesterol and triacylglycerol concentrations were markedly elevated in the proband and were classified as type IV hyperlipoproteinaemia. The plasma triacylglycerol concentration was moderately increased in a sister, who was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly), and in the son, who was a compound heterozygote for both mutant APOE alleles. Normal plasma lipid levels were observed in all other family members. In the plasma samples of the proband and his family members β-very-low-density lipoprotein was not detectable and the molar ratio of very-low-density lipoprotein-cholesterol to very-low-density lipoprotein-triacylglycerol was less than 0.9. The concentration of intermediate-density lipoprotein was within normal limits. 4. None of the family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) and/or APOE*2(Val-236→Glu) exhibited lipoprotein abnormalities characteristic of familial dysbetalipoproteinaemia, although three family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) showed hypertriglyceridaemia.

Plasma lipids, lipoproteins, and triglyceride turnover in eu- and hypo-thyroid rats and rats on a hypocaloric diet

1981 ◽  
Vol 59 (8) ◽  
pp. 715-721 ◽  
Author(s):  
Ladislav Dory ◽  
Brian R. Krause ◽  
Paul S. Roheim
Keyword(s):  
Half Life ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Caloric Intake ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Plasma Triglyceride ◽  
Low Density ◽  
Control Groups

Lipid and lipoprotein concentration, and triglyceride turnover were studied in control, thyroidectomized, and pair-fed control rats (pair-fed to match the food intake of the thyroidectomized rats). Thyroidectomy induced a significant increase in plasma cholesterol (and low density lipoprotein) concentrations and a decrease in plasma triglyceride (and very low density lipoprotein) concentrations. Changes in similar direction but of smaller magnitude were observed in the plasma of the pair-fed control rats. To further investigate triglyceride metabolism in these three groups of animals, triglyceride turnover was studied in fasted, unrestrained, and unanesthetized rats, following injection of [2-3H]glycerol. Peak incorporation of [2-3H]glycerol into plasma triglyceride occurred in all three groups of animals at 25 min after precursor administration, although the maximal incorporation was substantially lower in the thyroidectomized group than in either of the control groups. Thereafter, plasma triglyceride radioactivity decayed monoexponentially with a half-life of 24 ± 1 min for both normal and pair-fed control rats, compared with the half-life of 41 ± 3 min observed in the thyroidectomized rats. The calculated apparent fractional catabolic rates were thus 0.029 min−1 for both control groups and only 0.017 min−1 for the thyroidectomized animals. The apparent total catabolic rates of plasma triglyceride were 299 ± 11, 138 ± 11, and 48 ± 4 μg triglyceride∙min−1 for the normal controls, pair-fed controls, and thyroidectomized rats, respectively. These data further emphasize the importance of thyroid hormones in regulating plasma lipid and lipoprotein metabolism and, specifically, indicate that hypothyroidism results in a reduction of triglyceride secretion into, and the removal from, circulation. Furthermore, evidence was presented that the decreased caloric intake of the hypothyroid animals cannot, in itself, account for this observation.

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.

Abstract 20120: Protease-activated Receptor 4 Deficiency Reduces Atherosclerosis

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
A. Phillip Owens ◽  
Deborah A Howatt ◽  
Alan Daugherty ◽  
Nigel Mackman
Keyword(s):  
Mouse Model ◽  
Aortic Root ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Total Plasma Cholesterol ◽  
Total Plasma ◽  
Density Lipoprotein Receptor

Objective: Platelet activation is emerging as a critical process in both the formation and propagation of atherosclerosis. The coagulation protease thrombin activates platelets by cleavage of protease-activated receptor 4 (PAR4) in mice. Recent studies have demonstrated direct thrombin inhibitors reduce atherosclerosis in hypercholesterolemic mice. However, PAR4 deficiency had no effect on atherosclerosis in the apolipoprotein E (Apoe-/-) mouse model. The objective of this study was to re-examine the role of PAR4 deficiency in atherosclerosis using the alternative low-density lipoprotein receptor deficient mouse model. Methods and Results: To examine the effects of PAR4 deficiency on early atherosclerotic formation, low-density lipoprotein receptor deficient (Ldlr-/-) mice that were either PAR4+/+ (n = 11) or PAR4-/- (n = 12) were fed a fat-enriched diet (21% milk fat) and infused with angiotensin II (AngII; 1,000 ng/kg/min) for 28 days. PAR4 deficiency reduced AngII-induced aortic root atherosclerosis (+/+: 107 ± 22.1; -/-: 28.3 ± 7.50 μm2; P = 0.007). Bone marrow transplantation experiments were performed to determine the cellular source of PAR4 in atherosclerosis. Preliminary results demonstrate this reduction is dependent upon hematopoietic-derived PAR4 (+/+ into +/+: 230 ± 41; +/+ into -/-: 194 ± 23; -/- into +/+: 78 ± 18; and -/- into -/-: 68 ± 13 μm2; n = 4 each group; P < 0.02 +/+ hematopoietic versus -/- hematopoietic). PAR4 deficiency had no effects on total plasma cholesterol concentrations, lipoprotein-cholesterol distributions, or AngII increased systolic blood pressure. To determine the effects of a longer interval of diet-induced atherosclerosis, Ldlr-/-/PAR4+/+ (n = 12) or Ldlr-/-/PAR4-/- (n = 12) were fed a fat-enriched diet for 12 weeks. PAR4 deficiency attenuated aortic root atherosclerosis (+/+: 299 ± 15; -/-: 188 ± 18 μm2; P = 0.001) with no effects on total plasma cholesterol concentrations or lipoprotein distributions. Conclusion: We demonstrated that PAR4 deficiency resulted in an early (AngII: 74%) and late (Diet-induced: 37%) reduction in aortic root atherosclerosis. These results suggest that thrombin activation of PAR4 on platelets contributes to atherosclerosis in the Ldlr-/- model, but not the Apoe-/- model.

scholarly journals Focus on… Praluent®

2020 ◽  
pp. 175-178
Author(s):  
L Steyn
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pivotal Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein Receptors

Cholesterol plays a pivotal role in the functioning of healthy cells. Being mostly lipophilic, cholesterol is transported in the blood inside lipophilic particles, e.g. high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL). Hypercholesterolaemia refers to elevated low-density lipoprotein cholesterol (LDL-C) levels, and increases the risk for premature atherosclerotic cardiovascular disease (ASCVD). Low-density lipoprotein receptors (LDL-R) on the surface of hepatocytes, are the primary receptors involved in clearing circulating LDL-C.

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