Key result
Severe dyslipidemia series identifies universal APOE rs769452 T/T and ~40% APOC3 rs5128 carriage.
Why the study?
The study aimed to determine the presence of APOC3 rs5128, PON1 rs662, and APOE rs769452 genetic polymorphisms in patients with dyslipidemia and assess their significance for the nutrigenetic characterization of lipid metabolism disorders.
Observational (n=5)
This descriptive analysis of five dyslipidemia patients illustrates heterogeneity in lipid profiles and genetic variants (APOC3 rs5128 and PON1 rs662), suggesting that nutrigenetic interpretation requires integrating genetic findings with comprehensive clinical and metabolic profiling.
Should not alter dyslipidemia care; leaves open the nutrigenetic role of APOC3 rs5128, PON1 rs662, and APOE rs769452 variants.
ntroduction. To analyze clinical, laboratory, anthropometric, and molecular-genetic characteristics of patients with lipid metabolism disorders and to assess the potential significance of the APOC3 rs5128, PON1 rs662, and APOE rs769452 variants in the nutrigenetic interpretation of lipid phenotypes. The aim of the study. To determine the presence of the APOC3 rs5128, PON1 rs662, and APOE rs769452 genetic polymorphisms in patients with dyslipidemia and to assess their significance for the nutrigenetic characterization of lipid metabolism disorders. Materials and methods. We conducted a descriptive clinical-genetic analysis of five patients with lipid metabolism disorders. Sex, age, body mass index, total cholesterol, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, triglycerides, atherogenic coefficient, lipoprotein(a) level, and molecular-genetic results were assessed. Genotyping of APOC3 3238G >C (rs5128), PON1 575A >G (rs662), and APOE 3106T >C (rs769452) was performed by polymerase chain reaction. Results. The analysis included two men and three women, aged 29-57 years. The mean age was 40.8 years, and the mean body mass index was 28.4 kg/m². Mean total cholesterol was 7.19 mmol/L, low-density lipoprotein cholesterol 5.27 mmol/L, triglycerides 1.33 mmol/L, and the atherogenic coefficient was 4.45. Two patients had the APOC3 rs5128 G/C genotype, and three had the G/G genotype. For PON1 rs662, two patients had A/A, one had A/G, and two had G/G. All patients had the APOE rs769452 T/T genotype. Lipoprotein(a) levels were within reference ranges in all patients. Conclusions. The observations demonstrate heterogeneity in lipid metabolism disorders across anthropometric, laboratory, and genetic characteristics. The APOC3 rs5128 variant may be a potential modifier of triglyceride-rich lipoprotein metabolism, whereas PON1 rs662 may be related to variability in oxidative lipoprotein metabolism. Nutrigenetic interpretation should integrate genetic results with dietary assessment, body mass index, lipid profile, metabolic status, and overall cardiovascular risk.
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Zhurayev et al. (2026) conducted an observational in Dyslipidemia / lipid metabolism disorders (n=5). APOC3 rs5128, PON1 rs662, and APOE rs769452 genetic polymorphisms was evaluated on Presence of APOC3 rs5128, PON1 rs662, and APOE rs769452 genetic polymorphisms and lipid profile parameters. Genotyping of 5 dyslipidemia patients (mean LDL-C 5.27 mmol/L) showed 40% had APOC3 rs5128 G/C, 100% had APOE rs769452 T/T, and normal Lp(a) levels.
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