LOX-1 Gene Mapped in Medan: Majority of Population Carries the Heterozygous CT Genetic Variant

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FORMOSA NEWS - Medan - A recent genetic study has successfully mapped the variations of the LOX-1 gene among the population of Medan, North Sumatra. The research, published in 2026, was conducted by two Indonesian scientists: Shahrul Rahman from Universitas Muhammadiyah Sumatera Utara and Harun Al Rasyid from Universitas Sumatera Utara.

This study is highly significant because the LOX-1 gene plays a crucial role in detecting the risk of Nonalcoholic Fatty Liver Disease (NAFLD). This disease is a chronic liver disorder currently estimated to affect 20% to 30% of the global population. By mapping this genetic variation, the medical community moves one step closer to detecting and anticipating the risk of liver disease and cardiovascular complications early on a personalized level.

The Link Between Bad Cholesterol and Liver Damage

NAFLD can progress into a more aggressive condition known as Nonalcoholic Steatohepatitis (NASH). This condition triggers necroinflammatory activity, liver cell damage, and can eventually lead to liver cirrhosis and end-stage liver failure. Furthermore, patients at this stage face an escalated risk of developing diabetes mellitus and serious cardiovascular diseases.

Biologically, high circulating levels of oxidized low-density lipoprotein (oxLDL)—commonly known as bad cholesterol—act as a primary trigger for these systemic inflammatory cascades. The LOX-1 receptor in the body is responsible for binding and internalizing this bad cholesterol. However, when this cellular uptake becomes excessive, it induces intracellular reactive oxygen species (ROS) synthesis, accelerates cellular apoptosis, and sustains inflammation inside the hepatic tissues. Therefore, genetic variations in the LOX-1 gene directly influence how an individual's body responds to fat accumulation.

Laboratory Methodology and Blood Sample Testing

In this study, the research team enrolled 35 volunteer participants with a mean age of 43 years, consisting of 27 females and 8 males. To ensure accurate results without medical confounding backgrounds, the researchers applied rigid exclusion criteria. Individuals presenting with morbid obesity, clinical diabetes mellitus, overt dyslipidemia (high cholesterol), clinical thyroid dysfunction, or anomalies in copper metabolism were systematically excluded from the study population.

The testing process began by extracting genomic deoxyribonucleic acid (DNA) from peripheral blood leukocyte samples using the classic laboratory salting-out technique.

To profile the genetic variants of the LOX-1 gene specifically at the 3'UTR188C/T position, the researchers utilized the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) assay method. After enzymatic digestion with the RsaI restriction endonuclease, the restricted DNA fragments were visualized via ethidium bromide fluorescence under UV light to determine the specific alleles and genotypes of each individual. The research protocol received formal institutional review and ethical approval from the Health Research Ethics Committee of the Faculty of Medicine, Universitas Muhammadiyah Sumatera Utara.

Heterozygous CT Genotype Predominates Among Participants

Based on the genetic analysis, the researchers uncovered a compelling distribution of the LOX-1 gene variants within the investigated sample population in Medan:

• CT Genotype (Heterozygous): Detected in 15 participants, accounting for 43% of the total cohort.
• CC Genotype (Homozygous): Detected in 17 participants, accounting for 49% of the total cohort.
• TT Genotype (Homozygous): Detected in only 3 participants, accounting for 8% of the total cohort.

In terms of overall allelic frequency, the C allele (major variant) was highly predominant, appearing 47 times (67%). Conversely, the minor T allele was observed only 23 times (33%). This demonstrates that the heterozygous CT configuration is the most prevalent variant within this study cohort.

Benefits for Healthcare Policy and the Medical World

Shahrul Rahman and Harun Al Rasyid explained in their findings that the LOX-1 gene is hypothesized to indirectly aggravate the severity of hepatocyte injury in NASH by modulating the balance of pro- and anti-inflammatory adipokines. These adipokines are crucial regulators in progressive liver damage. When a person consumes a high-fat diet, certain genetic variations can trigger an unfavorable profile postprandially, characterized by a spike in pro-inflammatory cytokines (such as resistin) and a drop in protective, anti-inflammatory adipokines (such as adiponectin).

These findings carry significant implications for the future of medicine and public health policy in Indonesia:

1. Personalized Medicine: Clinicians can map a patient's genetic profile beforehand to determine their susceptibility to liver injury triggered by high-fat dietary intake, allowing for personalized therapy and rigorous monitoring.
2. Early Cardiovascular Prevention: Because the LOX-1 mutation is linked to the accumulation of atherogenic postprandial triglyceride-rich lipoproteins (TRLPs) in the vascular tracks, these results help identify individuals at a higher risk for cardiovascular diseases.
3. Data-Driven Public Education: Government bodies and educational institutions can leverage local genetic data to design more effective, targeted nutritional intervention campaigns for urban communities.

Researcher Profiles

Shahrul Rahman, S.Ked., M.Sc. – Lecturer and researcher at the Faculty of Medicine, Universitas Muhammadiyah Sumatera Utara (UMSU). Expert in medical biochemistry, human genetics, and healthcare analytics.

Dr. dr. Harun Al Rasyid, Sp.JP(K) – Academic staff member at Universitas Sumatera Utara (USU). Specialist in cardiology, vascular medicine, and biomolecular studies of chronic metabolic disorders.

Study Reference

Journal Article Title: Overview of LOX-1 Gen 3'UTR188C/T Polymorphism in Medan, Indonesia

Journal Name: Asian Journal of Healthcare Analytics (AJHA)
Publication Year: 2026
Official Digital Object Identifier (DOI): https://doi.org/10.55927/ajha.v5i1.16437

https://journal.formosapublisher.org/index.php/ajha