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Life sciences · Journal article
International Journal of Medical Science and Dental Health · September 22, 2026
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Background. Obesity is a multifactorial disease arising from interactions among environmental, behavioural, metabolic, and genetic factors. The leptin signalling system is a key component of the central regulation of energy balance. The rs1137100 polymorphism of the leptin receptor gene (LEPR) results in the Lys109Arg amino acid substitution and may be associated with variability in leptin sensitivity and the metabolic characteristics of obesity. However, findings vary considerably across populations. Objective. To evaluate the distribution of alleles and genotypes of the LEPR rs1137100 polymorphism in patients with overweight and obesity and to determine the associations between these genotypes and lipid metabolism, insulin resistance, and circulating leptin levels. Materials and Methods. The clinical cohort included 171 patients with overweight or obesity. Molecular genetic testing was performed in 74 patients (67 women and 7 men; mean age, 38.5 ± 1.4 years; mean body mass index [BMI], 37.7 ± 0.8 kg/m²). The control group consisted of 70 apparently healthy individuals with normal body weight (mean BMI, 22.6 ± 0.6 kg/m²). Genomic DNA was isolated from peripheral blood leukocytes using the NK-Magnit Base-96 kit. The rs1137100 polymorphism was genotyped using polymerase chain reaction followed by restriction fragment analysis. The A and G alleles and the A/A, A/G, and G/G genotypes were identified. The metabolic phenotype was assessed based on total cholesterol, low-density lipoprotein cholesterol, triglyceride and leptin concentrations, as well as the homeostatic model assessment of insulin resistance (HOMA-IR). Statistical analyses were performed using STATISTICA version 10.0 and Epi Info version 7.2.2.2. Results. The G/G genotype was identified in 32.4% of patients and 12.9% of controls (OR = 3.25; 95% CI, 1.42–7.44; p = 0.006, Fisher’s exact test). The frequency of the G/G genotype was 30.8% among patients with overweight or class I–II obesity and 36.4% among those with class III obesity; however, direct comparison according to obesity severity revealed no statistically significant differences. Within the patient group, the metabolic parameters progressively worsened across the A/A, A/G, and G/G genotypes. Compared with A/A carriers, G/G carriers had higher levels of low-density lipoprotein cholesterol (3.71 ± 0.05 vs 3.03 ± 0.04 mmol/L), triglycerides (2.23 ± 0.03 vs 1.64 ± 0.03 mmol/L), total cholesterol (5.81 ± 0.06 vs 4.95 ± 0.08 mmol/L), HOMA-IR (4.34 ± 0.04 vs 2.81 ± 0.05), and leptin (29.87 ± 0.80 vs 21.30 ± 0.90 ng/mL). Conclusion. In the study population, the G/G genotype of the LEPR rs1137100 polymorphism was associated with obesity and a more adverse metabolic phenotype. However, this genotype did not independently differentiate between obesity severity categories. These findings suggest that the G/G genotype may be considered a candidate marker of a metabolically adverse obesity phenotype, although confirmation in larger independent cohorts and multivariable models is required.