Increase of plasma proapolipoprotein A-I in patients with liver cirrhosis and its relationship to circulating high-density lipoproteins 2 and 3

1993 ◽  
Vol 39 (1) ◽  
pp. 60-65 ◽  
Author(s):  
T Suehiro ◽  
M Yamamoto ◽  
K Yoshida ◽  
F Ohno
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Density Lipoprotein ◽  
Normal Subjects ◽  
High Density ◽  
High Density Lipoproteins ◽  
Enzyme Linked Immunosorbent Assay ◽  
Converting Enzyme ◽  
Sandwich Method ◽  
The Mean

Abstract We determine the concentration of proapolipoprotein (proapo) A-I and its ratio with total apolipoprotein (apo) A-I (proapo A-I/total apo A-I) in plasma of patients with liver disease; we used a noncompetitive sandwich method, an enzyme-linked immunosorbent assay. The mean (SD) proapo A-I concentrations in patients with decompensated or compensated liver cirrhosis were higher than in normal subjects: 88 (25), 105 (36), and 69 (25) mg/L, respectively. The mean (SD) ratio (expressed as %) for each of these types of liver cirrhosis was also higher than in normal subjects: 10.0 (3.5), 10.2 (3.9), and 4.6 (1.6), respectively. In the patients, the proapo A-I concentration was positively correlated with the concentration of high-density lipoprotein subtype 2 cholesterol (HDL2-C) (r = 0.736), and the proapo A-I/total apo A-I ratio was correlated inversely with the HDL3-C concentration (r = -0.609). The activity of proapo A-I converting enzyme in patients with liver cirrhosis (62 +/- 30 nmol/h per liter) was significantly (P < 0.01) lower than that in normal subjects (172 +/- 55 nmol/h per liter). The increases of the plasma proapo A-I concentration and ratio in patients with liver cirrhosis may be caused by a decreased production of the converting enzyme in the liver. The increase of plasma proapo A-I may thus also affect the circulating HDL subtypes.

Determination of high-density lipoprotein phospholipids in serum.

1980 ◽  
Vol 26 (9) ◽  
pp. 1275-1277 ◽  
Author(s):  
Y Yamaguchi
Keyword(s):  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mean Value ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Color Development ◽  
The Mean

Abstract I describe a method for measuring high-density lipoprotein phospholipids. Magnesium chloride and dextran sulfate are used to precipitate all low-density and very-low-density lipoproteins. The supernate contains only high-density lipoproteins, the phospholipid concentration of which is determined by an enzymic method. The precision of the method (CV) is 2.35% (10 repeated assays), and the mean value for HDL-phospholipids was 1006 (SD 248) mg/L for 30 apparently healthy subjects. I used electrophoresis and enzymic color development to confirm the presence of HDL-phospholipids. Results are compared with those obtained by an ultracentrifugation method.

scholarly journals High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad and the Future

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 857
Author(s):  
Josep Julve ◽  
Joan Carles Escolà-Gil
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
Epidemiological Studies ◽  
High Density ◽  
High Density Lipoproteins ◽  
Atherosclerotic Cardiovascular Disease ◽  
Plasma High Density ◽  
Low Levels

Epidemiological studies have shown that low levels of plasma high-density lipoprotein cholesterol (HDL-C) are associated with increased atherosclerotic cardiovascular disease (CVD) [...]

scholarly journals High-Density Lipoproteins and the Kidney

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 764
Author(s):  
Arianna Strazzella ◽  
Alice Ossoli ◽  
Laura Calabresi
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Cholesterol Acyltransferase ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lcat Deficiency ◽  
Progression Of Renal Disease ◽  
The Impact

Dyslipidemia is a typical trait of patients with chronic kidney disease (CKD) and it is typically characterized by reduced high-density lipoprotein (HDL)-cholesterol(c) levels. The low HDL-c concentration is the only lipid alteration associated with the progression of renal disease in mild-to-moderate CKD patients. Plasma HDL levels are not only reduced but also characterized by alterations in composition and structure, which are responsible for the loss of atheroprotective functions, like the ability to promote cholesterol efflux from peripheral cells and antioxidant and anti-inflammatory proprieties. The interconnection between HDL and renal function is confirmed by the fact that genetic HDL defects can lead to kidney disease; in fact, mutations in apoA-I, apoE, apoL, and lecithin–cholesterol acyltransferase (LCAT) are associated with the development of renal damage. Genetic LCAT deficiency is the most emblematic case and represents a unique tool to evaluate the impact of alterations in the HDL system on the progression of renal disease. Lipid abnormalities detected in LCAT-deficient carriers mirror the ones observed in CKD patients, which indeed present an acquired LCAT deficiency. In this context, circulating LCAT levels predict CKD progression in individuals at early stages of renal dysfunction and in the general population. This review summarizes the main alterations of HDL in CKD, focusing on the latest update of acquired and genetic LCAT defects associated with the progression of renal disease.

Abstract 260: Knockout of Apolipoprotein A-II Has Dramatic Effects on High-Density Lipoprotein Subspecies Distribution

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Scott M Gordon ◽  
Catherine A Reardon ◽  
Godfrey S Getz ◽  
W S Davidson
Keyword(s):  
Gel Filtration ◽  
Density Lipoprotein ◽  
High Density ◽  
Paraoxonase 1 ◽  
High Density Lipoproteins ◽  
Ionization Mass ◽  
Associated Proteins ◽  
Compositional Diversity ◽  
The Impact ◽  
Modest Effect

High density lipoproteins (HDL) are a highly heterogeneous population of particles composed of various lipids and proteins. They have been demonstrated to possess a diverse variety of functional properties which are thought to contribute to protection against cardiovascular disease (CVD). Proteomics studies have identified up to 75 different proteins which can associate with HDL. The basis for the compositional diversity of HDL is not known but a better understanding will yield important information about its broad functional diversity. To investigate the impact of common HDL apolipoproteins on the distribution of other apolipoproteins, we have begun to systematically fractionate plasma from various HDL apolipoprotein KO mice. Plasma from apoA-I, apoA-IV and apoA-II global KO mice was applied to gel filtration chromatography to distinguish HDL size populations. HDL particles sequestered by a phospholipid binding resin were proteomically analyzed by electrospray ionization mass spectrometry. By comparing elution volume shifts (i.e. particle size variations) for each HDL protein between WT controls and the KO models, we assessed the impact of the deleted protein on HDL size distributions. Ablation of apoA-I, while decreasing total HDL phospholipid by 70%, had a surprisingly small impact on the distribution of the majority of other HDL associated proteins - affecting only 9 of them. Genetic apoA-IV ablation had a similar modest effect shifting a distinct subset of 9 proteins. However, loss of apoA-II, in addition to causing a similar 70% reduction in overall HDL phospholipids, affected the size distribution of some 45 HDL proteins (including several complement proteins and paraoxonase-1). These data suggest that apoA-I, while associated with the majority of HDL phospholipid, may actually interact with relatively few of the lower abundance proteins known to be associated with HDL. ApoA-II on the other hand, may interact with many of these, perhaps acting as a docking site or adaptor molecule.

Involvement of high-density lipoprotein in stimulatory effect of hormones supporting function of the bovine corpus luteum.

2003 ◽  
Vol 51 (1) ◽  
pp. 111-120 ◽  
Author(s):  
D. Skarżyński ◽  
J. Młynarczuk ◽  
J. Kotwica
Keyword(s):  
Luteinising Hormone ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Luteal Cells ◽  
Progesterone Secretion ◽  
Bovine Corpus Luteum ◽  
Progesterone Synthesis ◽  
Deficient Medium ◽  
Intracellular Pathway

The hypothesis that epinephrine (noradrenaline, NA) enhances utilisation of high-density lipoproteins (HDL) by bovine luteal cells and that this process involves phospholipase (PL) C and protein kinase (PK) C intracellular pathway was tested. Luteal cells from days 2-4, 5-10 or 11-17 of the oestrous cycle were pre-incubated for 20h. Subsequently DMEM/Ham's F-12 medium was replaced by fresh medium and the cells were treated for 6 h as follows: In Experiment I with HDL (5-75μg cholesterol per ml), NA, isoprenaline (ISO) or luteinising hormone (LH). In Experiment II cells were incubated for further 24h in deficient medium (without FCS) and next treated as in Experiment I. In Experiment III cells were stimulated with NA, ISO or LH alone and together with HDL. In Experiment IV cells were treated with PLC inhibitor (U-73122) or with PKC inhibitor (staurosporine) or stimulator (phorbol 12-myristrate 13-acetate) and with either NA, insulin or LH. Only luteal cells from days 5-10 of the cycle responded on HDL and β-mimetics (P<0.05). LH stimulated progesterone secretion from the luteal cells during all stages of the cycle (P<0.001). Cells incubated in deficient medium and supplemented with HDL secreted as much progesterone as those stimulated by LH in all stages of the cycle. Beta-mimetics were unable to enhance the stimulatory effect of HDL. Blockade of PLC had no influence on progesterone secretion from cells treated with either NA or LH, but this did impair the stimulatory effect of insulin (P<0.05). Similarly, blockade of PKC by staurosporine impaired (P<0.05) the effect of insulin only but not that observed after LH or NA treatment. We suggest that: (a) noradrenergic stimulation does not enhance utilisation of cholesterol from HDL for progesterone secretion; (b) the fasting of luteal cells seems to activate enzymes responsible for the progesterone synthesis; (c) effect of NA on progesterone secretion from luteal cells does not involve the PLC-PKC pathway.

scholarly journals Hypertriglyceridemia is associated with the incidence of preeclampsia

2018 ◽  
pp. 218-221
Author(s):  
Intje S Dahlan ◽  
Mardiah Tahir ◽  
Efendi Lukas ◽  
St. Maisuri T Chalid
Keyword(s):  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mean Value ◽  
High Density ◽  
University Teaching ◽  
Low Density ◽  
Hospital Department ◽  
Exact Test ◽  
The Mean

Abstract Objective: to find out  the correlation between lipid profille at trimester II of pregnancy and the incidence.of preeclampsia Method : The research  was conducted in the Polyclinic of Hasanuddin University Teaching Hospital, Department of Obstetrics and Gynecology of the Faculty of Medicine, and it network in Makassar city from March, 2015 through March, 2016. The research used was the prospective cohort design. Results : The examination of the lipid levels of 115 pregnant mothers, aged 24-28 weeks. The mothers were then observed whether they experienced preeclampsia up to the time they gave birth or not. In the end, 8 subjects (6.9%) experienced preeclampsia and 107 subjects (93.1%) have no preeclampsia. The statistical analyses used Fisher’s Exact test and Mann Whitney test. The research results indicated that the mean value of the total cholesterol and Low Density Lipoprotein (LDL) was higher in the preeclampsia group compared to the non-preeclampsia group: 267.37 ± 64.12 : 238 ± 37.98; 177.38 ± 55.38 : 157.24 ± 35.08 (p>0.05). The mean value of High Density Lipoprotein (HDL) was lower in the preeclampsia group compared to the non-preeclampsia group: 64.75 ± 14.64 : 67.86 ± 16.72 (p>0,05). The mean value of trigliserida in preeclampsia group was significantly higher (19,5%) compared thanin the non-preeclampsia group: 260.12 ± 58.86 vs 209.14 ± 65.10 (p=0,027). Conclusion : The hypertrigliseridemia was correlated with the preeclampsia incidence. Keywords:preeclampsia, lipid profile, trimester II of pregnancy   Abstrak Tujuan: mengetahui hubungan antara profil lipid kehamilan trimester II dengan kejadian preeklamsia. Metode : Penelitian dilaksanakan di Poliklinik RS jejaring pendidikan Departemen Obstetri dan Ginekologi Fakulltas Kedokteran Universitas Hasanuddin dan Poliklinik Kesehatan Ibu dan Anak di beberapa Puskesmas Kota Makassar selama Maret 2015 sampai dengan Maret 2016. Rancangan penelitian yang digunakan adalah prospektif  kohort. Hasil: dari 115 ibu hamil dilakukan pemeriksaan  kadar lipid, 115 ibu hamil pada usia kehamilan 24 – 28 minggu, kemudian diamati apakah subyek mengalami preeklamsia hingga proses persalinan. Terdapat delapan subyek (6,9%) berkembang menjadi preeklampsia dan 107 subyek tidak preeklamsia. Data dianalisis secara statistik dengan menggunakan uji Fisher’s Exact dan uji Mann Whitney. Hasil penelitian menunjukkan bahwa nilai mean kolesterol total dan Low Density Lipoprotein (LDL) lebih tinggi pada kelompok preeklampsia dibandingkan kelompok tidak preeklamsia, yaitu 267,37 ± 64,12 : 238,01 ± 37,98; 177,38 ± 55,38 : 157,24 ± 35,08 (p>0,05). Nilai mean High Density Lipoprotein (HDL) lebih rendah pada kelompok preeklamsia dibandingkan tidak preeklamsia yaitu 64,75 ± 14,64 : 67,86 ± 16,72 (p>0,05). Nilai mean trigli seri daripada kelompok preeklamsia secara signifikan lebih tinggi 19,5 % dibandingkan kelompok tidak preeklamsia, yaitu 260,12 ± 58,86 : 209,14 ± 65,10 (p=0,027). Kesimpulan : Hiper trigli seridemia berhubungan dengan kejadian preeklamsia. Kata kunci : preeklamsia, profil lipid, kehamilan trimester II    

scholarly journals Fontan‐Associated Dyslipidemia

2021 ◽  
Author(s):  
Adam M. Lubert ◽  
Tarek Alsaied ◽  
Joseph J. Palermo ◽  
Nadeem Anwar ◽  
Elaine M. Urbina ◽  
...  
Keyword(s):  
Liver Disease ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Fontan Circulation ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Reactive Protein

Background Hypocholesterolemia is a marker of liver disease, and patients with a Fontan circulation may have hypocholesterolemia secondary to Fontan‐associated liver disease or inflammation. We investigated circulating lipids in adults with a Fontan circulation and assessed the associations with clinical characteristics and adverse events. Methods and Results We enrolled 164 outpatients with a Fontan circulation, aged ≥18 years, in the Boston Adult Congenital Heart Disease Biobank and compared them with 81 healthy controls. The outcome was a combined outcome of nonelective cardiovascular hospitalization or death. Participants with a Fontan (median age, 30.3 [interquartile range, 22.8–34.3 years], 42% women) had lower total cholesterol (149.0±30.1 mg/dL versus 190.8±41.4 mg/dL, P <0.0001), low‐density lipoprotein cholesterol (82.5±25.4 mg/dL versus 102.0±34.7 mg/dL, P <0.0001), and high‐density lipoprotein cholesterol (42.8±12.2 mg/dL versus 64.1±16.9 mg/dL, P <0.0001) than controls. In those with a Fontan, high‐density lipoprotein cholesterol was inversely correlated with body mass index ( r =−0.30, P <0.0001), high‐sensitivity C‐reactive protein ( r =−0.27, P =0.0006), and alanine aminotransferase ( r =−0.18, P =0.02) but not with other liver disease markers. Lower high‐density lipoprotein cholesterol was independently associated with greater hazard for the combined outcome adjusting for age, sex, body mass index, and functional class (hazard ratio [HR] per decrease of 10 mg/dL, 1.37; 95% CI, 1.04–1.81 [ P =0.03]). This relationship was attenuated when log high‐sensitivity C‐reactive protein was added to the model (HR, 1.26; 95% CI, 0.95–1.67 [ P =0.10]). Total cholesterol, low‐density lipoprotein cholesterol, and triglycerides were not associated with the combined outcome. Conclusions The Fontan circulation is associated with decreased cholesterol levels, and lower high‐density lipoprotein cholesterol is associated with adverse outcomes. This association may be driven by inflammation. Further studies are needed to understand the relationship between the severity of Fontan‐associated liver disease and lipid metabolism.

THE RELATIONSHIP BETWEEN INFLAMMATION MARKERS AND MAGNESIUM/PHOSPHATE RATIO WITH ENDOTEL FUNCTION IN PERIPHERAL ARTERY DISEASE

2021 ◽  
Vol 6 (15) ◽  
pp. 80-86
Author(s):  
Serhat Çalışkan ◽  
Mehmet ATAY ◽  
Ferit BÖYÜK
Keyword(s):  
High Density Lipoprotein ◽  
Peripheral Artery Disease ◽  
Density Lipoprotein ◽  
High Density ◽  
Magnesium Phosphate ◽  
Peripheral Artery ◽  
The Mean ◽  
Endothelial Functions ◽  
Artery Disease ◽  
The Relationship

Objective: In our study, it was aimed to evaluate the relationship between neutrophil/lymphocyte, monocyte/high-density lipoprotein and magnesium/phosphate ratios with endothelial functions in patients with peripheral artery disease. Methods: Sixty patients followed up with peripheral arterial disease were included in this study. Endothelial functions of the patients were evaluated by flow-mediated vasodilation test. Pearson correlation analysis was used to evaluate the relationship between magnesium/phosphate, neutrophil/lymphocyte, monocyte/high-density lipoprotein ratios with percent change in flow-mediated vasodilation. Results: 48.3% of the participants are male and 51.7% are female. The mean age of the patients were 66.85±11.08 years. The mean radial artery basal diameter was 0.24±0.02 cm in the flow-mediated vasodilatation test and after the test the mean radial artery diameter was 0.27±0.02 cm(p<0.001). In the flow-mediated dilatation test predicting endothelial functions, the percentage change in arterial diameter was positively correlated with the Magnesium/phosphate ratio (r=-0.326, p=0.011), and negatively correlated with the Neutrophil/lymphocyte ratio and monocyte/high-density lipoprotein ratio (respectively r= -0.411, p=0.001; r=-0.530, p=0.001). Conclusion: Magnesium/phosphate ratio, neutrophil/lymphocyte ratio and monocyte/high-density lipoprotein ratio can be used to predict endothelial dysfunction in patients with peripheral artery disease.

Abstract 617: Intestine-Specific MTP Deficiency with ACAT2 Gene Ablation Lowers Acute Cholesterol Absorption With Chylomicrons and High-Density Lipoproteins

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Jahangir Iqbal ◽  
Mohamed Boutjdir ◽  
Lawrence L Rudel ◽  
M Mahmood Hussain
Keyword(s):  
Density Lipoprotein ◽  
Microsomal Triglyceride Transfer Protein ◽  
Cholesterol Absorption ◽  
High Density ◽  
High Density Lipoproteins ◽  
High Cholesterol ◽  
Intestinal Cholesterol Absorption ◽  
Triglyceride Accumulation ◽  
Abca1 Expression ◽  
Deficient Mice

Intestinal cholesterol absorption involves chylomicron and high density lipoprotein (HDL) pathways. Microsomal triglyceride transfer protein (MTP) and ATP binding cassette family A protein 1 (ABCA1) are critical for cholesterol transport by these pathways, respectively. Additionally, acyl Co-A:cholesterol acyltransferase 2 (ACAT2) plays an important role in cholesterol absorption. Intestinal MTP ablation significantly increased intestinal triglyceride and cholesterol levels and reduced their acute absorption. In contrast, ACAT2 deficiency had no effect on triglyceride absorption but significantly reduced cholesterol absorption. Individual deficiencies of ACAT2 and MTP reduced cholesterol absorption with chylomicrons. We hypothesized that their combined deficiency would increase cholesterol secretion with HDL; unexpectedly, their deficiency reduced secretion with both chylomicrons and HDL. Further, we observed significant reductions in intestinal ABCA1 expression in combined deficient mice. Thus, free cholesterol is unavailable for secretion by the HDL pathway in these mice. We speculate that reductions in ABCA1 expression and HDL secretion might be secondary to massive triglyceride accumulation associated with intestinal MTP deficiency. Besides its role in cholesterol absorption, ACAT2 deficiency causes mild hypertriglyceridemia and reduces steatosis in mice fed high cholesterol diets by increasing hepatic lipoprotein production by unknown mechanisms. We show that this phenotype is preserved in the absence of intestinal MTP in ACAT2 deficient mice fed a Western diet. Further, we observed increases in hepatic MTP activity in these mice. Thus, ACAT2 deficiency might increase MTP expression to avoid steatosis. Therefore, ACAT2 inhibition might avert steatosis associated with high cholesterol diets by increasing MTP expression.

Sign in / Sign up

Export Citation Format

Share Document