Abnormal concentrations of CII, CIII, and E apolipoproteins among apolipoprotein B-containing, B-free, and A-I-containing lipoprotein particles in hemodialysis patients

1991 ◽  
Vol 37 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Naji Alsayed ◽  
RegIs Rebourcet
Keyword(s):  
Total Cholesterol ◽  
Apolipoprotein B ◽  
Marked Decrease ◽  
Hemodialysis Patients ◽  
Serum Concentrations ◽  
Dialysis Patients ◽  
Apo B ◽  
Lipoprotein Particles ◽  
Apo E ◽  
Anephric Patients

Abstract Serum concentrations of total cholesterol, triglycerides, and apolipoproteins (apo) A-I, B, CII, CIII, and E in 36 hemodialysis patients and nine anephric patients were compared with the concentrations in 34 normolipidemic subjects. The dialysis patients displayed a moderate hypertriglyceridemia (1.94 +/- 0.12 vs 1.09 +/- 0.11 mmol/L in controls, mean +/- SEM; P less than 0.001), apo CIII concentrations were also increased (130.2 +/- 2.1 vs 108.4 +/- 0.7 mg/L; P less than 0.001), whereas apo CII (34.5 +/- 0.5 vs 36 +/- 0.5 mg/L; P less than 0.05), apo E (22.7 +/- 0.3 vs 27.9 +/- 0.2 mg/L; P less than 0.001), and apo A-I (1.18 +/- 0.05 vs 1.31 +/- 0.04 g/L; P less than 0.05) were decreased. Concentrations of serum apo B were normal (0.86 +/- 0.03 vs 0.97 +/- 0.07 g/L). In the hemodialysis patients, apo CIII concentrations were increased in apo B-containing lipoproteins (30.1 +/- 0.5 vs 25.0 +/- 0.1 mg/L; P less than 0.001), whereas CII and E were decreased below control values (14.4 +/- 0.2 vs 16.8 +/- 0.1, and 8.2 +/- 0.2 vs 11.4 +/- 0.1 mg/L, respectively; P less than 0.001 each). By calculation, non-B-containing lipoproteins in the hemodialysis group had increased concentrations of apo CIII (100.1 +/- 2.1 vs 83.3 +/- 0.7 mg/L; P less than 0.001) and decreased amounts of apo E (14.5 +/- 0.4 vs 16.4 +/- 0.3 mg/L; P less than 0.001); apo CII content was unchanged (20.1 +/- 0.5 vs 19.3 +/- 0.5 mg/L). Results for apo CII, CIII, and E among apo A-I-containing lipoproteins in both normolipidemic and hemodialysis groups were similar to those in non-B-containing lipoproteins. Finally, the sole significant (P less than 0.01) difference between the anephric and hemodialysis groups was the lower apo E concentrations in the former group. Accumulation of triglyceride-rich lipoproteins in hemodialysis patients may thus be related to the enrichment of apo CIII in apo B-containing lipoproteins and to a marked decrease in the apo CII and E contents.

scholarly journals Decreased Plasma Adiponectin Concentrations in Women with Dyslipidemia

2002 ◽  
Vol 87 (6) ◽  
pp. 2764-2769 ◽  
Author(s):  
Miyao Matsubara ◽  
Shoji Maruoka ◽  
Shinji Katayose
Keyword(s):  
Total Cholesterol ◽  
Body Fat ◽  
Fat Mass ◽  
Atherogenic Index ◽  
Body Fat Mass ◽  
Apo B ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Apo E ◽  
Wide Range

Adiponectin, the gene product of the adipose most abundant gene transcript 1, is a novel adipocyte-derived peptide that has been considered to have antiinflammatory and antiatherogenic effects. To characterize the relationship between adiponectin and lipids metabolism, we measured fasting plasma adiponectin concentration by ELISA, serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and apolipoprotein (apo) levels in 352 nondiabetic women, 16–86 yr old, with a wide range of body weight [body mass index (BMI), 14.8−36.3 kg/m2]. Plasma adiponectin concentrations in women with the highest tertile of TG (1.69 mm ≤ ∼) were decreased, compared with the middle (1.13 ≤ ∼ <1.69) or lowest tertile of TG (∼ <1.13) (5.9 ± 0.5 vs. 7.5 ± 0.3, 9.2 ± 0.2 μg/ml; P < 0.005, 0.001). Plasma adiponectin with the lowest tertile of HDL-C (∼ <1.16 mm) was decreased, compared with the middle (1.16 ≤ ∼ < 1.81) or highest tertile of HDL-C (1.81 ≤ ∼) (5.7 ± 0.5 vs. 7.8 ± 0.2, 10.1 ± 0.4 μg/ml; both P < 0.001). These relationships had similar tendencies after adjustment for BMI, body fat mass, age, or diastolic blood pressure. Adiponectin was negatively correlated with serum TG (r = −0.33, P < 0.0001), atherogenic index [(total cholesterol − HDL-C)/HDL-C] (r = −0.34, P < 0.0001), apo B (r = −0.45, P < 0.0001), or apo E (r = −0.29, P < 0.05), and positively correlated with serum HDL-C (r = 0.39, P < 0.0001) or apo A-I levels (r = 0.42, P < 0.002). Those negative relationships became stronger after adjusting for BMI or body fat mass. The slightly positive correlation between adiponectin and age, blood urea nitrogen, or creatinine levels was also observed (all P < 0.001). These results indicate that high-TGnemia and low-HDL-Cnemia are associated with low plasma adiponectin concentrations in nondiabetic women. Further efforts must now be targeted to determine whether adiponectin causes these lipid abnormalities and thus whether it is partly responsible for the atherogenic risk seen in the metabolic syndrome.

scholarly journals Response of Homocysteine, Cystathionine, and Methylmalonic Acid to Vitamin Treatment in Dialysis Patients

2005 ◽  
Vol 51 (1) ◽  
pp. 196-201 ◽  
Author(s):  
Rima Obeid ◽  
Martin K Kuhlmann ◽  
Hans Köhler ◽  
Wolfgang Herrmann
Keyword(s):  
Folic Acid ◽  
Vitamin B6 ◽  
Methylmalonic Acid ◽  
Treatment Strategies ◽  
Treatment Phase ◽  
Hemodialysis Patients ◽  
Current Treatment ◽  
Serum Concentrations ◽  
Dialysis Patients ◽  
Baseline Serum

Abstract Background: Hyperhomocysteinemia is observed in >80% of hemodialysis patients and is considered a risk factor for cardiovascular disease. Vitamin treatment lowers total homocysteine (tHcy) concentrations in plasma and may therefore reduce the associated risk. Current treatment strategies have not achieved normalization of tHcy in the majority of dialysis patients. Methods: We administered folic acid (5 mg) plus vitamin B6 (50 mg) and B12 (0.7 mg) intravenously to 38 hyperhomocysteinemic patients (tHcy >18 μmol/L) after each dialysis treatment. The treatment phase lasted 1 month, and serum concentrations of tHcy, methylmalonic acid (MMA), and cystathionine were measured at weeks 0, 2, 4, 6, 8, and 24. Results: The median serum tHcy concentration decreased significantly, from 26.1 μmol/L at baseline to 13.2 μmol/L at week 4. The median change in tHcy after 4 weeks was 13.4 μmol/L (−51%) compared with baseline. Serum MMA and cystathionine concentrations were reduced by 28% and 26%, respectively, but neither was normalized at 4 weeks. Backward-elimination stepwise regression analysis revealed that higher concentrations of tHcy, MMA, and cystathionine and lower folate at baseline predict changes of tHcy after treatment. Twenty weeks after vitamin withdrawal, tHcy concentrations returned to values comparable to baseline (median, 24.8 μmol/L). Conclusions: The combination of folic acid, vitamin B12, and vitamin B6 used in this study normalized serum concentrations of tHcy in almost all of our hyperhomocysteinemic dialysis patients. This regimen may be used to investigate the effects of homocysteine normalization on cardiovascular outcomes in hemodialysis patients.

Report of Dialysis-Induced Hypophosphatemia Leading to Reversible Encephalopathy Prevented by Adding Phosphorus to the Dialysate

2020 ◽  
Vol 49 (4) ◽  
pp. 496-501
Author(s):  
Divya Koganti ◽  
Ramin Sam
Keyword(s):  
Hemodialysis Patients ◽  
High Serum ◽  
Serum Phosphorus ◽  
Phosphorus Concentration ◽  
Serum Concentrations ◽  
Dialysis Patients ◽  
Sharp Decline ◽  
Advanced Chronic Kidney Disease ◽  
Extracellular Compartment ◽  
Reversible Encephalopathy

Patients with advanced chronic kidney disease have an inability to excrete phosphorus normally leading to high serum concentrations of phosphorus. The hyperphosphatemia is even more pronounced in dialysis patients who often require large doses of phosphorus binders to combat the problem. Hemodialysis is able to remove fair amount of the extra phosphorus; however, the removal is often hampered by the fact that the phosphorus is removed only from the extracellular compartment and phosphorus is mainly intracellular. The end result being a high serum phosphorus concentration at the beginning of dialysis, a sharp decline in the value by the end of dialysis and significant rebound of serum phosphorus concentration a few hours after stopping dialysis as phosphorus moves out of the cells. Here, we describe 2 hemodialysis patients with normal predialysis serum phosphorus concentration and preexisting conditions that made them at risk for developing encephalopathy who developed recurrent obtundation toward the end of the dialysis treatments. After confirming critical postdialysis hypophosphatemia, phosphorus was added to the dialysate baths and the episodes of encephalopathy associated with dialysis ceased.

Tunicamycin induces ubiquitination and degradation of apolipoprotein B in HepG2 cells

2001 ◽  
Vol 353 (3) ◽  
pp. 493-501 ◽  
Author(s):  
Wei LIAO ◽  
Lawrence CHAN
Keyword(s):  
Apolipoprotein B ◽  
Hepg2 Cells ◽  
Proteasome Inhibitor ◽  
Plasma Lipoproteins ◽  
Apo B ◽  
Net Production ◽  
Lipoprotein Particles ◽  
Essential Component ◽  
Intracellular Degradation

Apolipoprotein (apo) B-100 is an essential component of atherogenic plasma lipoproteins. Previous studies have demonstrated that the production of apoB-100 is regulated largely by intracellular degradation at both the co-translational and post-translational levels and that proteasome-mediated and non-proteasome-mediated pathways are involved in this process. ApoB-100 is a glycoprotein. The present study was undertaken to address the question of whether the inhibition of N-linked glycosylation with tunicamycin would interfere with apoB-100 production. We demonstrated that the treatment of HepG2 cells with tunicamycin decreased the net production of apoB-100 by enhancing co-translational degradation of the protein. This effect of tunicamycin was partly prevented by lactacystin, a specific proteasome inhibitor. Because lactacystin only partly reversed the effects of tunicamycin on apoB biogenesis, tunicamycin seemed also to induce apoB co-translational degradation in HepG2 cells by one or more non-proteasomal pathways. Furthermore, tunicamycin increased apoB ubiquitination approx. 4-fold. The proportion of the newly synthesized apoB-100 that was secreted and incorporated into the nascent lipoprotein particles was unaffected by tunicamycin. Thus the tunicamycin-mediated inhibition of N-linked glycosylation interferes with the production of apoB-100 that is mediated by both proteasomal and non-proteasomal pathways.

Aggregation of Human Blood Platelets by Remnant Like Lipoprotein Particles of Plasma Chylomicrons and Very Low Density Lipoproteins

1997 ◽  
Vol 77 (05) ◽  
pp. 0996-1001 ◽  
Author(s):  
Abby R Saniabadi ◽  
Kazou Umemura ◽  
Makiko Shimoyama ◽  
Masakazu Adachi ◽  
Minoru Nakano ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Platelets ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Red Cell ◽  
Very Low Density Lipoproteins ◽  
Apo B ◽  
Unbound Fraction ◽  
Lipoprotein Particles ◽  
Apo E

SummaryRemnant like lipoprotein particles (RLP) of partially catabolised human plasma chylomicrons (CM) and very low density lipoproteins (VLDL) were separated from CM and VLDL using two monoclonal antibodies, anti apo B-100 (JI-H) and anti apo A-I (H-12) coupled to Sepharose 4B gel to form an immunoaffinity column. Lipoproteins containing apo B-100 or apo E, including VLDL and LDL adsorb to (JI-H)-gel, while CM and HDL with apo A-I adsorb to (H-12)-gel. The unbound fraction (RLP) is rich in apo B-48, apo E and apo E rich apo B-100 which has not been recognized by JI-H. The RLP fraction with a total triglyceride of 12.35 ± 6.22 mg/ml; total cholesterol, 0.32 ± 0.08 mg/ml and total protein, 0.72 ± 0.12 mg/ml (mean ± S.E.M, n = 9) was added to blood from healthy persons at 2.5-200 |xl/ml and agitated gently at 37° C for 40 s. Platelet aggregation was assessed by measuring the loss of single platelets. At 2.5-10 μl, RLP induced platelet aggegation increased with the dose of RLP, but decreased at 25-200 julL Scanning electron microscopy revealed that within 20 s of agitation in the presence of RLP, activated platelets had appeared on the red cell membrane and within 40 s of agitation, platelet aggregates had formed on the red cells. The platelet responses were unaffected by aspirin (10 or 20 μg/ml) but were inhibited by cilostazol, a phosphodiesterase type III inhibitor (0.4 to 1.6 μg/ml). It is likely that the platelet effect of RLP is a consequence of RLP dependent red cell-platelet interaction. This is the first report of platelet aggregation induced by RLP without an added platelet agonist.

Serum concentrations of apolipoprotein A-I, apolipoprotein B, and lipoprotein(a) in a population sample

1995 ◽  
Vol 41 (11) ◽  
pp. 1633-1636 ◽  
Author(s):  
A Leino ◽  
O Impivaara ◽  
M Kaitsaari ◽  
J Järvisalo
Keyword(s):  
Apolipoprotein B ◽  
Population Sample ◽  
Serum Concentrations ◽  
Finnish Population ◽  
Apo B ◽  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Increased Risk ◽  
Age Dependent ◽  
Age And Sex

Abstract Serum concentrations of apolipoprotein (apo) A-I, apo B, and lipoprotein(a) [Lp(a)] were studied with respect to age and sex in a Finnish population sample of 575 subjects (286 men and 289 women), ages 27-67 years. Apo A-I and apo B were measured with an immunoturbidimetric method calibrated against WHO International Reference Materials. Lp(a) was measured by RIA. Apo A-I and apo B concentrations were almost normally distributed (apo A-I: mean 1.38 g/L vs median 1.34 g/L for men, and 1.58 g/L vs 1.55 g/L for women; apo B: mean 1.21 g/L vs median 1.20 g/L for men and 1.09 g/L vs 1.05 g/L for women). The distribution of Lp(a) was remarkably skewed (mean 190 mg/L vs median 86 mg/L for men, and 169 mg/L vs 85 mg/L for women). The 95% intervals for apo A-I were 1.09-1.84 g/L for men and 1.06-2.28 g/L for women; for apo B, they were 0.63-1.88 g/L and 0.56-1.82 g/L, respectively. Apo A-I concentrations appeared to be unrelated to age, whereas apo B and Lp(a) concentrations were age-dependent. Cutoff values based on the 90th percentile for apo B and the 10th percentile for apo A-I are proposed for identifying subjects at increased risk of coronary heart disease.

Precipitation of apo E-containing lipoproteins by precipitation reagents for apolipoprotein B.

1984 ◽  
Vol 30 (11) ◽  
pp. 1784-1788 ◽  
Author(s):  
J C Gibson ◽  
A Rubinstein ◽  
W V Brown
Keyword(s):  
Apolipoprotein B ◽  
Dextran Sulfate ◽  
Manganese Concentration ◽  
High Density Lipoproteins ◽  
Apo B ◽  
Heparin Concentration ◽  
Agarose Beads ◽  
Apo E ◽  
Before And After ◽  
Lipoprotein Association

Abstract We measured the solubility of apolipoprotein E (apo E) after precipitation, with heparin-Mn2+ or dextran sulfate-Mg2+, of lipoproteins containing apo B. Data from 46 randomly selected subjects suggest that apo E is readily precipitated by dextran sulfate-Mg2+, but that heparin-Mn2+ preferentially precipitates apo E associated with apo B-containing lipoproteins while leaving the apo E-containing fraction of high-density lipoproteins (HDL) in solution. In a more detailed analysis of three subjects, we measured the lipoprotein association of apo E by column chromatography on agarose beads, before and after its precipitation from plasma. This study confirmed the preferential solubility of apo E associated with HDL lipoproteins. Using plasma from two normolipidemic subjects, we maintained the heparin concentration at 1.30 g/L and varied the manganese concentration from 9.2 to 184 mmol/L. A 46 mmol/L concentration best separated apo E-containing HDL from apo B-containing lipoproteins. Thus, at these final concentrations, heparin-Mn2+ appears to precipitate the apo E associated with apo B-containing lipoproteins, leaving soluble most of the apo E associated with lipoproteins of HDL size.

scholarly journals AB0562 POTENTIAL BIOMARKERS OF PERSONALIZED TREATMENT BASED ON CARDIOVASCULAR-RELATED COMORBIDITIES IN PSORIATIC ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1317.2-1318
Author(s):  
I. Arias de la Rosa ◽  
M. D. López Montilla ◽  
C. Román-Rodriguez ◽  
I. Gómez García ◽  
M. J. Pérez Galán ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Disease Activity ◽  
Total Cholesterol ◽  
Body Mass ◽  
Apolipoprotein B ◽  
Combined Therapy ◽  
Pde4 Inhibitor ◽  
Apo B

Background:Psoriatic Arthritis (PsA) displays increased traditional cardiovascular (CV) risk factors, such as insulin resistance (IR), metabolic syndrome or obesity. Thus, it is an urgent need to treat and manage these cardiometabolic comorbidities associated. Some evidence points out that methotrexate could improve CV risk due to its anti-inflammatory properties, however the effect of PDE4 inhibitor treatment on CV risk have not been elucidated yet.Objectives:1) To evaluate the effect of conventional therapy and PDE4 inhibitor in PsA patients with high prevalence of cardiometabolic comorbidities. 2) To identify a molecular patient profile susceptible of being benefit from each therapy regarding disease activity and CV risk.Methods:Thirty biological-naïve patients with PsA were treated with the PDE4 inhibitor (Apremilast), Methotrexate or combined therapy (Apremilast and Methotrexate) following the clinical routine practice for 6 months. A cohort of 30 age and sex-matched healthy donors (HDs) was included. Plasma and peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of patients and HDs. Different parameters related to the cardiometabolic risk were analyzed, including: atherogenic index, ratio apolipoprotein B (apo B)/apolipoprotein A (apo A), insulin resistance (IR), metabolic syndrome, obesity, arterial hypertension, and the SCORE. Clinical and analytical parameters were collected: lipid profile (total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, apo A and apo B), glucose and insulin, body surface area (BSA) affected by psoriasis, number of tender and swollen joints, DAPSA, C-reactive protein and erythrocyte sedimentation rate. A panel of 92 proteins involved in cardiovascular disease (cardiovascular panel II, Olink) and an adipocytokine profile was measured in plasma and PBMCs. Hard cluster analysis was carried out in order to identify two distinctive molecular phenotypes depending on the treatment response related to the reduction of CV risk.Results:Among the 92 CV-related proteins, the higher levels of two molecules, CD163 and FABP4 observed in PsA patients compared to HDs, were strongly associated with elevated rates of CV risk factors such as apolipoprotein B/A and atherogenic risks, metabolic syndrome, obesity, IR, arterial hypertension and smoking. Thus, we could identify two clinical profiles of patients according to the plasma levels of these molecules: cluster 1 defined by 20 patients with low levels of CD163 and FABP4 and low prevalence of CV comorbidities and cluster 2 defined by 10 patients with high levels of CD163 and FABP4 and high prevalence of CVD comorbidities. Regarding cluster 2, those patients that were treated with Apremilast or combined therapy had a significant reduction of CD163 and FABP4 associated with a drop in total cholesterol, apo B, IR state and body mass index. In addition, both PDE4 inhibitor and combined treatment reduced activity disease. However, Methotrexate in monotherapy did not show a beneficial effect in PsA patients displaying higher levels of CD163, FABP4, total cholesterol and no changes in disease activity after treatment. In regard to cluster 1, the three therapy strategies reduced disease activity after 6 months. Even with low rates of comorbidities, those patients treated with Apremilast had reduced levels of total cholesterol and apolipoprotein B and body mass index after 6 months of therapy. However, no changes were observed in the treatment with Methotrexate or Methotrexate combined with Apremilast.Conclusion:1- CD163 and FABP4 could be considered as potential biomarkers of treatment efficacy regarding cardiometabolic comorbidities. 2- Apremilast might target metabolic alterations in PsA modulating lipid profile, insulin resistance and body mass index, decreasing the levels of surrogate CV-related molecules. 3- Apremilast treatment should be considered in PsA patients with higher rates of cardiometabolic comorbidities.Funded by ISCIII (PI17/01316 and RIER RD16/0012/0015) co-funded with FEDER.Disclosure of Interests:None declared.

Lipoprotein(a) in Korean Children and a History of Coronary or Cerebral Vascular Events in Their Older Family Members

1997 ◽  
Vol 34 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Yon H Choe ◽  
Yong Choi ◽  
Jin Q Kim
Keyword(s):  
Body Weight ◽  
Family History ◽  
Total Cholesterol ◽  
Geometric Mean ◽  
Obese Group ◽  
Serum Concentrations ◽  
Vascular Events ◽  
Apo B ◽  
Lipoprotein A ◽  
History Of

The purpose of this study was to determine the relationships between serum apolipoprotein concentration and family history of coronary or cerebral events in schoolchildren. In 269 primary schoolchildren aged 6–11 years (145 boys and 124 girls) we measured the blood concentrations of total cholesterol, apolipoproteins B and A-1, and lipoprotein(a), and questioned their parents about coronary or cerebral vascular events. Serum concentrations of apo B, A-1 and Lp(a) significantly increased with age. In children with serum cholesterol concentration > 5·18 mmol/L the concentrations of apo B, A-1, Lp(a) and apo B/apo A-1 ratio were significantly higher. The concentrations of total cholesterol, apo B, Lp(a), and apo B/apo A-1 ratio in the obese group (body weight 20% above the median body weight for age and height) differed significantly from those in the non-obese group. Serum concentrations of Lp(a) in the children who had positive family histories of coronary or cerebral events (geometric mean = 0·174 × / ÷ 0·036g/L) and was significantly higher than that in the children with negative history (geometric mean = 0·086 × / ÷ 0·36g/L). Family history was an independent and major contributor to high Lp(a). In evaluating children's lipid profiles, measurement of Lp(a) may help to identify children and their families at increased risk and this may facilitate the targeting of preventive measures.

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