Objective: Low-molecular weight (MW) apolipoprotein(a) [apo(a)] isoforms are closely associated with an increased incidence of atherothrombotic disease, prevalence of which is higher in obese individuals, particularly in women. The hypothesis of this study was to assess whether there are differences in the distribution of apo(a) phenotypes between obese patients and healthy controls.
Research Methods And Procedures: One hundred three obese Italian women (BMI > or = 30.0 kg/m2) were enrolled in the study, and apo(a) phenotyping was performed in all subjects. The prevalence of low-MW apo(a) isoforms, detected in plasma samples of our obese women, was compared with that found in a control group of 84 normal-weight, never-obese (BMI < 25.0 kg/m(2)), age-matched women.
Results: The distribution of apo(a) isoforms in the population of obese women was significantly different from that found in normal-weight female subjects. In particular, the percentage of subjects in the obese group with at least one apo(a) isoform of low MW was significantly higher than that in the control group (51.4% vs. 32.1%, p = 0.0079).
Discussion: Our results seem to suggest the possibility that small-sized apo(a) isoforms may be used together with other traditional risk factors to better assess the overall predisposition to atherothrombotic disease in obese women.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1038/oby.2004.166 | DOI Listing |
J Clin Lipidol
December 2024
Center for the Prevention of Cardiovascular Disease, Leon H. Charney Division of Cardiology, Department of Medicine, NYU Grossman School of Medicine. 530 First Avenue, HCC5, New York, NY 10016, USA. Electronic address:
Background: Lipoprotein(a) [Lp(a)] is a driver of residual cardiovascular risk. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) decrease Lp(a) with significant heterogeneity in response. We investigated contributors to the heterogeneous response.
View Article and Find Full Text PDFJ Lipid Res
December 2024
Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN, USA. Electronic address:
J Intern Med
December 2024
Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria.
Background: Lipoprotein(a) (Lp(a)) is a causal, genetically determined risk factor for cardiovascular disease (CVD) in the general population. Patients with chronic kidney disease (CKD) have an increased CVD risk and elevated Lp(a) concentrations. Only a few studies on Lp(a) were performed in persons with mild-to-moderate CKD; none of them used genetic variants to explore potential causal associations.
View Article and Find Full Text PDFEur J Prev Cardiol
January 2025
VA Palo Alto Healthcare System, 3801 Miranda Avenue, Palo Alto, CA, 94304, USA.
Aims: Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease, but the mechanisms of risk are debated. Studies have found inconsistent associations between Lp(a) and measurements of atherosclerosis. We aimed to assess the relationship between Lp(a), low-density lipoprotein cholesterol (LDL-C), and coronary artery plaque severity.
View Article and Find Full Text PDFJVS Vasc Sci
June 2024
Department of Medicine, Division of Preventive Medicine and Nutrition, Columbia University Vagelos College of Physicians and Surgeons, New York, NY.
Background: High lipoprotein (a) [Lp(a)] is associated with adverse limb events in patients undergoing lower extremity revascularization. Lp(a) levels are genetically pre-determined, with gene encoding for two apolipoprotein (a) [apo(a)] isoforms. Isoform size variations are driven by the number of kringle IV type 2 (KIV-2) repeats.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!