J Obes Metab Syndr.
2024 Sep;33(3):213-221. 10.7570/jomes23064.
Associations of the PPARα and Lipoprotein Lipase Enzyme Gene Polymorphisms with Dyslipidemia in Obese and Non-obese Males
- Affiliations
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- 1Department of Clinical Biochemistry, College of Pharmacy, University of Al-Ameed, Karbala, Iraq
- 2Department of Clinical Biochemistry, College of Medicine, Kufa University, Najaf, Iraq
- KMID: 2559979
- DOI: http://doi.org/10.7570/jomes23064
Abstract
- Background
Peroxisome proliferator-activated receptor α (PPARα) is a nuclear transcription factor responsible for gene expression, particularly those associated with lipid metabolism. The lipoprotein lipase enzyme (LPL) is considered a key enzyme in lipid metabolism and transport. The link between dyslipidemia and obesity is well understood. Dyslipidemia is also an established risk feature for cardiovascular disease. Thus, it becomes progressively essential to identify the role of genetic factors as risk markers for the development of dyslipidemia among obese males.
Methods
A case-control study was performed including 469 males. Anthropometric characteristics and serum lipid profiles such as triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were evaluated. Genomic DNA extraction and purification were performed using whole blood samples. Restriction enzyme fragment length polymorphism was used to genotype PPARα and LPL single nucleotide polymorphisms. The associations between these polymorphisms and dyslipidemia were examined.
Results
The CC and CG genotypes of PPARα gene polymorphisms were significantly associated with higher TC and LDL-C levels (P<0.05). The TT genotype of the LPL gene polymorphism was significantly associated with higher TG levels and lower HDL-C levels (P<0.05). In contrast, the GG genotype may have a protective action against dyslipidemia.
Conclusion
The study reaches the interesting conclusion that there was a significant association between PPARα as well as LPL gene polymorphisms and dyslipidemia among obese and non-obese males.
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