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Updated: Apr 17, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Rhesus monkey (Macaca mulatta) lipoprotein(a) and apolipoprotein(a): high frequency of small size apolipoprotein(a)
Byambaa Enkhmaa1, Adnan Abbuthalha1, Erdembileg Anuurad1
1Department of Internal Medicine, University of California, Davis, CA, USA.
Background:
Levels of lipoprotein(a), Lp(a), a genetically regulated independent cardiovascular risk factor present in humans and Old World monkeys, are impacted by the apolipoprotein(a), apo(a), gene. Allele-specific apo(a) levels, taking both the apo(a) genotypic and phenotypic characteristics into account, are useful markers to determine atherosclerotic cardiovascular risk.
Methods:
We determined (i) the genetic variability of apo(a), (ii) Lp(a) levels, and (iii) allele-specific apo(a) levels in rhesus monkeys (n = 95).
Results:
Lp(a) levels differed substantially between animals (range: 4-247 nmol/l) with a skewed distribution toward lower levels. Lp(a) and allele-specific apo(a) levels were inversely related to the number of apo(a) Kringle 4 (K4) repeats. The median apo(a) size was 23 K4 repeats, and the prevalence of a small size apo(a) (≤22 K4) was 43%.
Conclusions:
Distribution of Lp(a) and allele-specific apo(a) levels in rhesus monkeys reflected the corresponding human patterns, but with a high prevalence of smaller apo(a) sizes.
Insights
Lipoprotein(a) levels in rhesus monkeys mirror human patterns, with smaller apolipoprotein(a) sizes being more common. These findings offer insights into cardiovascular risk assessment.
Area of Science:
- Genetics and Molecular Biology
- Cardiovascular Disease Research
- Primate Models in Medicine
Background:
- Lipoprotein(a) [Lp(a)] is a genetically regulated cardiovascular risk factor.
- The apolipoprotein(a) [apo(a)] gene influences Lp(a) levels.
- Allele-specific apo(a) levels are valuable markers for atherosclerotic cardiovascular risk.
Purpose of the Study:
- To investigate the genetic variability of apo(a) in rhesus monkeys.
- To determine Lp(a) levels and allele-specific apo(a) levels in this population.
- To compare these findings with human patterns for cardiovascular risk assessment.
Main Methods:
- Analysis of genetic variability of the apo(a) gene in 95 rhesus monkeys.
- Quantification of Lp(a) levels using established biochemical assays.
- Determination of allele-specific apo(a) levels, considering genotypic and phenotypic characteristics.
Main Results:
- Significant inter-animal variation in Lp(a) levels (4-247 nmol/l) was observed.
- Lp(a) and allele-specific apo(a) levels showed an inverse correlation with apo(a) Kringle 4 (K4) repeat number.
- The median apo(a) size was 23 K4 repeats, with 43% of monkeys having small apo(a) (≤22 K4 repeats).
Conclusions:
- The distribution of Lp(a) and allele-specific apo(a) levels in rhesus monkeys aligns with human patterns.
- A high prevalence of smaller apo(a) sizes was noted in the studied rhesus monkey population.
- Rhesus monkeys serve as a relevant model for studying Lp(a) and apo(a) in the context of cardiovascular risk.
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