A Longitudinal Genetic Study of Plasma Lipids in Adolescent Twins

2007 ◽  
Vol 10 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Rita P. S. Middelberg ◽  
Nicholas G. Martin ◽  
John B. Whitfield
Keyword(s):  
Total Cholesterol ◽  
Environmental Effects ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Environmental Influences ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Lipids And Lipoproteins ◽  
Adolescent Twins ◽  
Over Time

AbstractPlasma lipids such as high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol and triglyceride levels contribute to variation in the risk of cardiovascular disease. The early stages of atherosclerosis in childhood have also been associated with changes in triglycerides, LDL and HDL. Heritability estimates for lipids and lipoproteins for adolescents are in the range .71 to .82, but little is known about changes of genetic and environmental influences over time in adolescence. We have investigated the contribution of genetic and environmental influences to variation in lipids in adolescent twins and their nontwin siblings using longitudinal twin and family data. Plasma HDL and LDL cholesterol, total cholesterol and triglycerides data from 965 twin pairs at 12, 14 and 16 years of age and their siblings have been analyzed. Longitudinal genetic models that included effects of age, sex and their interaction were fitted to assess whether the same or different genes influence each trait at different ages. Results suggested that more than one genetic factor influences HDL, LDL, total cholesterol and triglycerides over time at ages 12, 14 and 16 years. There was no evidence of shared environmental effects except for HDL and little evidence of long-term nonshared environmental effects was found. Our study suggested that there are developmental changes in the genes affecting plasma lipid concentrations across adolescence.

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.

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.

Effects of exercise training on plasma lipids and lipoproteins in rats

1985 ◽  
Vol 58 (2) ◽  
pp. 612-618 ◽  
Author(s):  
A. E. Pels ◽  
T. P. White ◽  
W. D. Block
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Plasma Lipids ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Oxidative Capacity ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Exercise Induced ◽  
Lipids And Lipoproteins

We studied the effects of exercise training on plasma lipid and lipoprotein concentrations of rats on a high-fat and high-cholesterol diet. Twelve weeks of training occurred at moderate [Mod-Exer, 70% peak O2 consumption (VO2)] and high (High-Exer, 82% peak VO2) intensities. The duration of daily training sessions was adjusted to maintain equivalent energy expenditure between groups. Following training, body weight and lean body mass were 10% lower in the High-Exer group than the Mod-Exer or control groups. Compared with control values, carcass fat content was 33% lower for both trained groups. The oxidative capacity of skeletal muscle was approximately 30% greater in the trained groups compared with the control group. Total cholesterol, high density lipoprotein cholesterol, and total triglyceride concentrations in plasma were not different between the trained groups, but were 33–47% lower compared with the control group. The exercise-induced changes in plasma lipid and lipoprotein concentrations may be a result of a change in preferred substrate utilization in skeletal muscle toward a greater oxidation of lipid.

Abstract P192: Lipoprotein(a) is Significantly Associated with ApoB-containing Atherogenic Lipoproteins in African Americans

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Enkhmaa Byambaa ◽  
Anuurad Erdembileg ◽  
Wei Zhang ◽  
Lars Berglund
Keyword(s):  
African Americans ◽  
Total Cholesterol ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Sandwich Elisa ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Lipoprotein A ◽  
Interethnic Difference

Background: Lipoprotein(a), Lp(a), is a genetically regulated independent cardiovascular risk factor, where levels differ across ethnicity. The relationship between Lp(a) and apolipoprotein B (apoB)-containing atherogenic lipoproteins across ethnicity is not well understood. Objective: To investigate the associations of Lp(a) levels with other apoB-containing lipoproteins with a focus on ethnicity. Methods: Plasma lipid and lipoproteins were measured in 336 Caucasians and 224 African Americans undergoing coronary angiography. Lp(a) levels were determined using an apo(a) size insensitive sandwich ELISA. Values for Lp(a) and triglyceride (TG) were square root or logarithmically transformed before analyses. Total and low density lipoprotein (LDL) cholesterol, and apoB levels were corrected for contribution of Lp(a) using previously published algorithms. Values are given mean ± standard deviation or median (interquartile range) for normally or non-normally distributed variables, respectively. Results: Levels of total and LDL cholesterol and apoB-100 did not differ between Caucasians and African Americans. As expected, African Americans had significantly higher levels of Lp(a) [110 (60-180) nmol/l vs. 24 (7-79) nmol/l, p<0.001] and high density lipoprotein (HDL) cholesterol (49±17 mg/dl vs. 41±12 mg/dl, p<0.001), as well as significantly lower levels of TG [106 (80-144) mg/dl vs. 153 (114-222) mg/dl, p<0.001] compared to Caucasians. For both ethnic groups, Lp(a) levels were significantly and positively correlated with total cholesterol (p<0.005 for Caucasians and p<0.001 for African Americans), LDL cholesterol (p<0.001 for both groups), apoB100 (p<0.05 for Caucasians and p<0.001 for African Americans) and apoB/apoA-1 ratio (p<0.05 for Caucasians and p<0.001 for African Americans). However, when adjusted for the corresponding contribution of Lp(a) to the levels of these parameters, the associations remained significant in African Americans (p<0.05 for total cholesterol; p<0.05 for LDL cholesterol; p<0.001 for apoB100, respectively), but not in Caucasians. Conclusion: Although total and LDL cholesterol, and apoB100 levels were comparable in African Americans and Caucasians, the associations of these parameters with Lp(a) levels differed across ethnicity. For African Americans, but not for Caucasians, associations of all three parameters with Lp(a) remained significant after appropriate adjustments. The findings suggest an interethnic difference in the relation between Lp(a) and other plasma apoB-containing lipoprotein levels, with a closer relationship among African Americans.

Abstract 197: Characterization of the Effects of Angiopoietin-Like 3 on Plasma Lipids and Lipoproteins in Humans

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Jessica Minnier ◽  
Sergio Fazio ◽  
Michael Shapiro ◽  
Sotirios Tsimikas ◽  
Marcello Arca ◽  
...  
Keyword(s):  
Total Cholesterol ◽  
Plasma Levels ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Multivariate Adaptive Regression Splines ◽  
Low Density ◽  
Lipid Phenotype ◽  
Ldl Size ◽  
Critical Reduction

Angiopoietin-like 3 (ANGPTL3) deficiency due to loss-of-function (LOF) gene mutations causes familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes and compound heterozygotes, with a lipid phenotype much milder in heterozygotes. We aim to determine whether a critical reduction in plasma ANGPTL3 levels is a major determinant of FHBL2 lipid phenotype. We studied 126 subjects from 19 families with ANGPTL3 LOF mutations. Individuals homozygous for mutations in ANGPTL3 manifest the full FHBL2 phenotype of reduced total cholesterol, triglycerides, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol (-C) and particle concentration (-p), and LDL size. Heterozygotes only displayed with low total cholesterol, HDL-C, HDL-p and VLDL-p compared with non-carriers. Using multivariate adaptive regression splines, we found that: ( i ) total cholesterol, triglycerides, LDL-C, HDL-C, HDL-p, and LDL size correlated with ANGPTL3 but only for levels below 25% of normal (<60 ng/dl); ( ii ) VLDL-p and LDL-p correlate with ANGPTL3 irrespective of its plasma levels; and ( iii ) homozygotes exhibited reduced levels of mature proprotein convertase subtilisin/kexin type 9 (PCSK9), a known regulator of plasma LDL-C levels. These results indicate that the full FHBL2 phenotype seen in homozygous carriers of LOF mutations in ANGPTL3 is caused by a critical reduction of more than 75% of its plasma levels, thus uncovering the relationship between mutation status, plasma ANGPTL3 concentrations, and the lipid phenotype. Furthermore, our study suggests that the low plasma LDL seen in homozygous carriers of ANGPTL3 LOF mutations is mediated by the modulation of plasma PCSK9.

The Effect of Low Molecular Weight Dextran Infusions on Plasma Lipids and Lipoproteins

1970 ◽  
Vol 38 (2) ◽  
pp. 233-244 ◽  
Author(s):  
T. P. Whitehead ◽  
P. W. Dykes ◽  
J. Gloster ◽  
P. Harris
Keyword(s):  
Molecular Weight ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Plasma Concentrations ◽  
Extracellular Fluid ◽  
Density Lipoprotein ◽  
Low Molecular Weight ◽  
Low Density ◽  
Dextran 40 ◽  
Lipids And Lipoproteins

1. Infusions of Dextran 40 induced a pronounced fall in the plasma concentration of cholesterol, in the absence of marked changes in plasma volume. Similar falls occurred in the plasma concentrations of phospholipids, triglyceride and low density lipoprotein. It was further observed that the return to normal was slow, and at 15 days was still incomplete. 2. Lipoprotein turnover studies failed to demonstrate altered rates of catabolism or evidence for altered synthetic rates. They were better interpreted in terms of redistribution from the plasma to the rest of the extracellular fluid, although there was no indication as to its exact site.

Angiopeptin Inhibition of Myointimal Hyperplasia after Balloon Angioplasty of Large Arteries in Hypercholesterolaemic Rabbits

1993 ◽  
Vol 85 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Marcus H. Howell ◽  
Michael M. Adams ◽  
Mary S. Wolfe ◽  
Marie L. Foegh ◽  
Peter W. Ramwell
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Balloon Catheter ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Low Density ◽  
Infrarenal Aorta ◽  
Cholesterol Diet ◽  
Elevated Plasma ◽  
Wide Range

1. Currently, a wide range of drugs is being evaluated for the ability to prevent the restenosis which frequently accompanies percutaneous transluminal coronary angioplasty. Patients undergoing angioplasty are generally hypercholesterolaemic and therefore the possibility that plasma lipids may compromise the efficacy of anti-restenotic drugs must be assessed. A promising drug in several clinical trials for the prevention of restenosis is angiopeptin, an octapeptide analogue of somatostatin that possesses a highly lipophilic terminal. 2. The effect of angiopeptin on myointimal hyperplasia was studied in a rabbit model of arterial balloon catheter injury where the rabbits were made hypercholesterolaemic by a 0.5% cholesterol diet. The degree of subsequent myointimal thickening was measured by morphometry. 3. Angiopeptin (20 μg day−1 kg−1) significantly inhibited myointimal thickening by an average of 47% in the infrarenal aorta and both the common and external iliac arteries in the presence of elevated plasma lipids concentrations. Low dose angiopeptin (2 μg day−1 kg−1) significantly inhibited myointimal thickening in the external iliac artery but not in the other two vessels. 4. Angiopeptin treatment (20 μg day−1 kg−1) did not significantly modify the plasma cholesterol, very-low-density lipoprotein, intermediate-sized low-density lipoprotein, low-density lipoprotein and high-density lipoprotein concentrations that were elevated by the 0.5% cholesterol diet. 5. We conclude that the inhibitory effect of angiopeptin is largely unaffected by elevated plasma lipid concentrations and that this drug did not modify plasma lipid concentrations in rabbits.

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.

Effects of exercise accumulation on plasma lipids and lipoproteins

2015 ◽  
Vol 40 (5) ◽  
pp. 441-447 ◽  
Author(s):  
Jason D. Wagganer ◽  
Charles E. Robison ◽  
Terry A. Ackerman ◽  
Paul G. Davis
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Random Order ◽  
Blood Lipid ◽  
Lipoprotein Cholesterol ◽  
Exercise Session ◽  
Significant Treatment ◽  
Lipid Panel ◽  
Lipids And Lipoproteins

Debate exists as to whether improvements in some cardiometabolic risk factors following exercise training result more from the last session of, or from an accumulation of, exercise sessions. This study was designed to compare the effect of a single exercise session with 3 consecutive days of exercise on triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C). Twelve young adult (aged 22.5 ± 2.5 years), overweight (body mass index = 29.7 ± 4 kg·m–2), sedentary, black (n = 5) and white (n = 7) men (n = 6) and women (n = 6) completed, in random order, a single treadmill exercise session at 60% maximal oxygen uptake for 90 min (1EX), accumulated exercise sessions (same as for 1EX) for 3 consecutive days (3EX), and a control protocol (no exercise for 6 days). Plasma samples were collected from baseline through 24, 48, and 72 h postexercise. Significant treatment-by-time interactions (p < 0.05) existed in HDL-C and LDL-C. Postexercise responses of HDL-C differed at 48 h (1EX: –3.6, 3EX: + 3.7 mg·dL−1) and 72 h (1EX: –1.7, 3EX: + 3.2 mg·dL−1). LDL-C responses differed at 48 h (1EX: –16, 3EX: + 6 mg·dL−1). Although not statistically significant, TG concentrations decreased by 29% at 24 h after 3EX, compared with –7% after 1EX. An inverse relationship between baseline and postexercise reduction in TG was present with 3EX (r = –0.655; p < 0.05). In conclusion, 3EX increased HDL-C and decreased TG more than 1EX, while the decrease in LDL-C after 1EX was suppressed. Blood lipid panel changes may be due to more accumulated effects over time rather than just a result of the most recent exercise session.

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.

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