Apolipoprotein B (apo B) signal peptide length polymorphisms are associated with apo B, low density lipoprotein cholesterol, and glucose levels in Mexican Americans

1996 ◽  
Vol 120 (1-2) ◽  
pp. 37-45 ◽  
Author(s):  
Candace M. Kammerer ◽  
John L. VandeBerg ◽  
Steven M. Haffner ◽  
James E. Hixson
2016 ◽  
Vol 14 (2) ◽  
pp. 36-40 ◽  
Author(s):  
Arabinda Mohan Bhattarai ◽  
HS Batra ◽  
Suchit Bandyopadhyay ◽  
Pratibha Misra ◽  
Manushri Sharma ◽  
...  

Introduction: Atherosclerotic Coronary Artery Disease (CAD) is fundamentally related to disorders of lipid metabolism. Health problems like obesity, glucose intolerance and metabolic syndrome increase atherosclerotic CAD risk.  A fraction of Low density lipoprotein cholesterol (LDL) is called small dense low density lipoprotein cholesterol (sdLDL). These particles are more atherogenic because they are taken up more easily by arterial wall, readily oxidized and not easily cleared from plasma. Every LDL particle contain an Apo B molecule.Methods: In this cross sectional study we recruited 100 known cases each of CAD, type 2 diabetes, overweight and 100 age and sex matched healthy controls. We took a detailed case summary along with anthropometric measurements. We measured sdLDL by heparin magnesium precipitation method followed by direct estimation of the LDL in the supernatant.Result: Linear regressive analysis showed positive correlation between sdLDL and Apolipoprotein B (Apo B) with LDL cholesterol (r=0.61, p=0.004), (r=0.754, p=0.0034) respectively. Multiple Comparisons after Kruskalwallis test of sdLDL and Apo B levels of  type 2 diabetes, CAD and overweight with controls were significant (p<0.001).Conclusion: Our findings suggest that the estimation of sdLDL and Apo B provide a complimentary benefit in assessment of cases with CAD, type 2 diabetes and overweight.


2012 ◽  
Vol 15 (3) ◽  
pp. 292-308 ◽  
Author(s):  
Christopher C. Imes ◽  
Melissa A. Austin

Coronary heart disease (CHD) affects 17 million people in the United States and accounts for over a million hospital stays each year. Technological advances, especially in genetics and genomics, have changed our understanding of the risk factors for developing CHD. The purpose of this article is to review low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), and risk of CHD. The article focuses on five topics: (1) a description of lipoprotein classes, normal lipoprotein metabolism, and the biological mechanism of atherosclerosis; (2) a review of selected epidemiologic and clinical trial studies examining the associations between elevated LDL-C and apo B with CHD; (3) a brief review of the familial forms of hyperlipidemia; (4) a description of variants in genes that have been associated with higher LDL-C levels in candidate gene studies and genome-wide association studies (GWAS); and (5) nursing implications, including a discussion on how genetic tests are evaluated and the current clinical utility and validity of genetic tests for CHD.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Seth S Martin ◽  
Atif N Qasim ◽  
Daniel J Rader ◽  
Muredach P Reilly

Introduction: Accumulating evidence suggests that apolipoprotein B (apoB) is superior to low-density lipoprotein cholesterol (LDL-C) in prediction of cardiovascular events. Yet, an important outstanding question is whether apoB, relative to LDL, is an enhanced marker for subclinical atherosclerosis, particularly in diabetics where LDL levels may underestimate atherogenic lipid burden due to increased proportion of small, dense LDL. Hypothesis: We hypothesized that plasma apoB would be a better predictor than LDL-C of coronary artery calcification (CAC) scores in type 2 diabetics and non-type 2 diabetics. Methods: We performed cross-sectional analyses of asymptomatic Caucasians in (1) The Study of Inherited Risk of Coronary Atherosclerosis (434 men and 383 women; median age 48, non-diabetics) and (2) The Penn Diabetes Heart Study (580 men and 261 women; median age 60, type 2 diabetics). Results: Levels of apoB and LDL-C were correlated in diabetics (r=0.78, p<0.001) and non-diabetics (r=0.77, p<0.001). There was no association between LDL-C and CAC in diabetics. In non-diabetics, an association of LDL-C was lost after adjustment for total cholesterol. In contrast, after controlling for age, gender, statin therapy, and total cholesterol, levels of apoB were positively associated with CAC in diabetics [tobit regression ratio for 30 mg/dl increase in apoB 2.94 (95% CI 1.62 – 5.53), p=0.001) and had a more modest association with CAC in non-diabetics [1.67 (95% CI 1.16 – 2.32), p=0.005]. Conclusions: ApoB, but not LDL-C, predicted CAC scores, a measure of coronary atherosclerotic burden. The strength of this association was greater in diabetics than non-diabetics. Relative to LDL-C, plasma apoB levels may be particularly useful in assessing CVD risk in type 2 diabetes.


1985 ◽  
Vol 31 (10) ◽  
pp. 1654-1658 ◽  
Author(s):  
S Marcovina ◽  
D France ◽  
R A Phillips ◽  
S J Mao

Abstract We produced 20 mouse monoclonal antibodies against human plasma low-density lipoprotein (LDL). Individually they failed to precipitate LDL in agarose gel by the double-immunodiffusion technique; collectively they did, or as few as two combined monoclonal antibodies could do so. To mimic polyclonal antibodies in determination of apolipoprotein B (apo B) by radial immunodiffusion, a combination of four particular monoclonal antibodies (clones A, B, C, and D) was necessary. We characterized these four clones with respect to temperature dependency, affinity, total binding to 125I-labeled LDL, and specificity to the different species of apolipoprotein B. Two monoclonal antibodies (B and C) bound 100% of 125I-labeled LDL; clones A and D bound 80% and 87%, respectively. All four clones bound maximally to LDL at 4 degrees C. The affinity constants for clones A, B, C, and D were 0.6, 2.1, 3.8, and 2.3 X 10(9) L/mol, respectively. By the Western blotting technique, the four monoclonal antibodies all reacted with the species B-100 and B-74 of apolipoprotein B, and to various degrees with B-48 and B-26. Radial immunodiffusion (chi) and direct enzyme-linked immunosorbent assay (y) with a mixture of the four monoclonal antibodies gave almost identical results for 70 patients: y = 0.921 chi-2.58; r = 0.933.


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