scholarly journals Asupan Gizi dan Kadar Low Density Lipoprotein Kolesterol Darah pada Kalangan Eksekutif

2013 ◽  
Vol 8 (2) ◽  
pp. 72
Author(s):  
Ratna Djuwita
Keyword(s):  
Food Frequency Questionnaire ◽  
Protein Intake ◽  
Nutrient Intake ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Animal Protein ◽  
Low Density ◽  
Food Frequency ◽  
24 Hour Recall

Kemajuan teknologi dan ekonomi akhir-akhir ini memberikan dampak perubahan pola hidup yang menyebabkan pergeseran pola penyakit. Terlihat pada peningkatan penyakit kardiovaskular pada kelompok eksekutif usia produktif. Hiperkolesterolemia adalah satu-satunya faktor risiko yang dapat menyebabkan timbulanya aterosklerosis. Asupan gizi terkait erat dengan hiperkolesterolemia. Tujuan penelitian ini adalah mengetahui hubungan antara asupan gizi serta pola makan dengan hiperkolesterolemia pada kalangan eksekutif di Jakarta. Desain penelitian adalah potong lintang. Populasi penelitian adalah kelompok eksekutif Indonesia dewasa berusia 25-60 tahun. Sampel penelitian terdiri dari 280 responden ber- usia 25-60 tahun yang merupakan kelompok eksekutif dari beberapa perusahaan yang ada di sekitar Jakarta. Kadar low density lipoprotein (LDL) kolesterol diperiksa dengan mengumpulkan sampel darah puasa. Asupan gizi dinilai dengan metode 24 hour recall dan pola makan dinilai dengan metode food frequency questionnaire (FFQ). Prevalensi hiperkolesterolemia pada kalangan eksekutif 46,1%. Prevalensi hiperkolesterolemia ini lebih tinggi secara bermakna pada laki-laki (50,9%) dibandingkan pada perempuan(29,7%). Prevalensi hiperkolesterolemia cenderung lebih tinggi pada kalangan eksekutif yang berumur di atas 40 tahun, berpendidikan tinggi dan berpenghasilan tinggi. Asupan gizi, khususnya protein hewani serta frekuensi mengonsumsi sapi, memiliki hubungan dengan prevalensi hiperkolesterolemia. Asupan protein nabati, kekerapan mengonsumsi tempe, asupan serat serta kekerapan mengonsumsi sayur dan buah dapat dipertimbangkan sebagai makanan yang protektif atau dapat menurunkan kadar LDL kolesterol dalam darah.Technology and economical development recently poses impact toward changes of lifestyle which cause shifted of the disease pattern. The escalating of cardiovascular appears to be more common among executive productive age group. Hypercholesterolemia is the only risk factor that by itself can cause atherosclerosis. Hypercholesterolemia might be influenced by nutrient intake. The objective of this study is to know the relationship of between nutrient intake as well as food pattern and hypercholesterolemia among executive group surrounding Jakarta. Low density lipoprotein (LDL) content was assessed by collecting fasting blood samples. 24 hour recall and food frequency questionnaire (FFQ) was conducted to assess nutrient intake. Prevalence hypercholesterolemia was 46.1% among this excecutive group.The prevalence of hypercholesterolemia was significant higher among men (50.6%) compared to women (29.7%). Hypercholesterolemia prevalence tend to be higher among those who were over 40 years old, had higher education and had higher income. There was a relationship between nutrient intake especially animal protein intake as well as more frequent consuming beef with the prevalence of hypercholesterolemia. Non-animal protein intake, more frequent consuming tempe, fibre intake as well as more frequent consuming fruit and vegetable might be considered as protective food toward lowering effect of the LDL plasma cholesterol level.

Abstract 566: MicroRNA-146a Deficiency Prevents PCSK9 Gain-of-Function Mutation-induced Hypercholesterolemia in Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Shayan Mohammadmoradi ◽  
Aida Javidan ◽  
Weihua Jiang ◽  
Jessica Moorleghen ◽  
Venkateswaran Subramanian
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Western Diet ◽  
Size Exclusion ◽  
Gel Chromatography ◽  
Low Density ◽  
Distribution Analysis ◽  
Gain Of Function ◽  
Ldl Particles

Background and Objective: Mimetic mediated activation of microRNA 146a (miR-146a) reduces atherosclerosis via suppression of nuclear factor-κB-driven inflammation in mice. The purpose of this study was to determine whether miR-146a influences plasma cholesterol in hypercholesterolemic mice. Methods and Results: To induce hypercholesterolemia, female C57BL/6 miR-146a WT (n=8) and miR-146a KO (n=8) mice were injected intraperitoneally with an adeno-associated viral vector (AAV) expressing the proprotein convertase subtilisin/kexin type 9 (PSCK9 D377Y) gain-of-function mutant at a dose of 3 x 10 10 genomic copies/mouse. After infection, mice were fed a Western diet (21% wt/wt milk fat; 0.15% wt/wt cholesterol) for sixteen weeks, and plasma PCSK9 and total cholesterol concentrations were monitored monthly using an enzymatic assay. Plasma PCSK9 concentrations were profoundly increased 4 weeks post injection (Baseline: WT - 179 ± 12 vs KO - 207 ± 12; Week 4: WT - 1700 ± 148 vs KO - 2689 ± 305 ng/ml) and remained significantly high during 16 weeks (WT - 882 ± 142 vs KO - 718 ± 109 ng/ml; p<0.05 vs baseline) of Western diet feeding. Consistent with increased plasma PCSK9 concentrations, plasma cholesterol concentrations were increased in both groups of mice. Interestingly, miR-146a KO group mice showed less significant increase in plasma cholesterol compared to WT group (Baseline: WT - 88 ± 3 vs KO - 83 ± 3; Week 4: WT - 328 ± 25 vs KO - 195 ± 18 mg/dl) irrespective of the comparable plasma PCSK9 concentrations. Also, lipoprotein distribution analysis with size exclusion gel chromatography revealed that miR-146a KO mice showed a strong reduction in high density lipoprotein (HDL) particles while very low density lipoprotein (VLDL) and low density lipoprotein (LDL) particles were not affected. Conclusion: Our findings suggests that miR146a plays a critical role in the regulation of HDL particles in PCSK9 gain-of-function mutant-induced hypercholesterolemia in mice. Future studies will identify gene targets influenced by miR-146a in regulating HDL-cholesterol in hypercholesterolemic mice.

Plasma lipoprotein profiles of normocholesterolemic and hypercholesterolemic homozygotes for apolipoprotein E2(Arg158-->Cys) compared

1994 ◽  
Vol 40 (8) ◽  
pp. 1559-1566 ◽  
Author(s):  
S P Zhao ◽  
A H Smelt ◽  
A M Van den Maagdenberg ◽  
A Van Tol ◽  
T F Vroom ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Plasma Cholesteryl Ester ◽  
Familial Dysbetalipoproteinemia ◽  
Lipoprotein Profiles

Abstract We compared plasma lipoprotein profiles of 15 individuals with normocholesterolemic (plasma cholesterol 4.81 +/- 0.90 mmol/L) familial dysbetalipoproteinemia (NFD) and 15 patients with hypercholesterolemic (plasma cholesterol 10.61 +/- 2.32 mmol/L) familial dysbetalipoproteinemia (HFD), matched for age and sex. All subjects were homozygous for apoE2(Arg158--&gt;Cys). Compared with 15 normolipidemic controls (plasma cholesterol 5.47 +/- 0.92 mmol/L), subjects with NFD and HFD had greater cholesterol concentrations of large very-low-density lipoprotein (VLDL1), small VLDL (VLDL2), and intermediate-density lipoprotein, each of which was correlated to their plasma total cholesterol concentration. VLDL1 and VLDL2 subfractions were enriched in cholesteryl ester, and plasma cholesteryl ester transfer protein activities were increased in both NFD and HFD; however, absolute changes were larger in HFD than in NFD. Concentrations of low-density lipoprotein cholesterol were lower in HFD (1.89 +/- 0.48 mmol/L) and NFD (1.56 +/- 0.36 mmol/L) than in normolipidemic controls (3.35 +/- 0.73 mmol/L). We conclude that all subjects homozygous for apoE2(Arg158--&gt;Cys) show features of dysbetalipoproteinemia.

scholarly journals The Effect of Quail Egg and Hen Egg Consumption on Low-Density Lipoprotein Oxidation and Small Dense Low-Density Lipoprotein

2020 ◽  
Author(s):  
Raveenan Mingpakanee ◽  
Chatchanok Chaisitthichai ◽  
Nattaporn Wichitamporn ◽  
Paradee Sappittayakorn ◽  
Suparnnikar Phongphanwatana
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lag Time ◽  
Plasma Triglyceride ◽  
Ldl Oxidation ◽  
Low Density ◽  
Egg Consumption ◽  
Hen Egg ◽  
Lipoprotein Profiles

Objective: The aim of the study was to investigate the effect of quail egg and hen egg supplements on lipoprotein profiles, low-density lipoprotein (LDL) oxidation and small dense LDL cholesterol (sd-LDL-C) in young healthy people, compared with hen eggs. Material and Methods: Twenty-three healthy volunteers (11 men and 12 women) were randomly assigned to consume 3 whole hen eggs per day (hen group, n=11) (total cholesterol 633 mg) or 9 quail eggs per day (quail group, n=12) (total cholesterol 459 mg) for 30 days. The plasma cholesterol and plasma triglyceride concentrations and lipoprotein fractions (Triglyceride-rich lipoprotein; TRL, LDL and high-density lipoprotein; HDL) were determined at baseline and after the 30-day period of egg consumption. The LDL oxidation (lag time) was measured by the increase of conjugated diene production. Sd-LDL-C was calculated from the major lipid and lipoprotein parameters. Results: In the quail group, plasma triglyceride (TG) and LDL-TG were significantly decreased, whereas the plasma cholesterol and HDL-C were unchanged. There was no alteration in lipoprotein profiles in the hen group. The LDL lag time of the quail group was longer than at baseline. There were no significant changes in sd-LDL-C levels in both groups during the study.Conclusion: Quail egg and hen egg consumptions for 30 days did not change the lipoprotein profiles, sd-LDL as well as the LDL-oxidation, which not modified the cardiovascular disease risk factor.

scholarly journals Loss of TIMP4 (Tissue Inhibitor of Metalloproteinase 4) Promotes Atherosclerotic Plaque Deposition in the Abdominal Aorta Despite Suppressed Plasma Cholesterol Levels

2021 ◽  
Author(s):  
Mei Hu ◽  
Sayantan Jana ◽  
Tolga Kilic ◽  
Faqi Wang ◽  
Mengcheng Shen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Thoracic Aorta ◽  
Abdominal Aorta ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Plaque Deposition ◽  
Cholesterol Levels

Objective: Atherosclerosis is accumulation of lipids and extracellular matrix in the arterial wall. TIMPs (tissue inhibitor of metalloproteinases) can impact plaque deposition by regulating ECM (extracellular matrix) turnover. TIMP4 also influences lipid metabolism and smooth muscle cell (SMC) proliferation. We investigated the role of TIMP4 in atherosclerosis. Approach and Results: Mice lacking low-density lipoprotein receptor ( Ldlr −/− ) and Timp4 ( Timp4 −/− / Ldlr −/− ) were fed high-fat diet (HFD) or regular laboratory diet. After 3 or 6 months, HFD-fed male and female Timp4 −/− / Ldlr −/− mice exhibited higher plaque density in the abdominal aorta (but not in aortic valves, arch, thoracic aorta) compared with Ldlr −/− mice. Although plasma lipid and cholesterol levels were lower in Timp4 −/− / Ldlr −/− -HFD, cholesterol content in the abdominal aorta was higher along with elevated inflammatory cytokines, MMP (matrix metalloproteinase) activities, CD68 + /calponin + macrophage-like SMCs in Timp4 −/− / Ldlr −/− -HFD compared with Ldlr −/− -HFD mice. In vitro, oxidized LDL (low-density lipoprotein) markedly increased CD68 expression, reduced SMC markers, increased lipid uptake, and reduced cholesterol efflux protein ABCA1 (ATP-binding cassette transporter A1) in Timp4 −/− / Ldlr −/− compared with Ldlr −/− primary SMCs from abdominal, but not thoracic aorta. TIMP4 expression in the abdominal aorta (in vivo) and its corresponding SMCs (in vitro) was ≈2-fold higher than in the thoracic aorta and SMCs; TIMP4 levels decreased following HFD. Timp4 -deficiency in bone marrow–derived macrophages did not alter their foam cell formation capacity. Conclusions: TIMP4 protects against plaque deposition in the abdominal aorta independent of plasma cholesterol levels. TIMP4 prevents proteolytic degradation of ABCA1 in SMCs, hindering cholesterol accumulation and transdifferentiation to macrophage-like foam cells, representing a novel negative regulator of atherosclerosis.

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