GP222 Clinical and metabolic parameters in girls-carriers of LEPR rs1137100 with android and gynoid obesity

Leptin is a peptide hormone of adipose tissue regulating energy metabolism. Numerous studies indicate LEPR gene contribution to obesity. There are no data on the role of LEPR gene rs1137100 polymorphism in development of android and gynoid types of obesity. Aim To compare the clinical and metabolic parameters in adolescent girls with android and gynoid obesity types - carriers of different genotypes of LEPR gene rs1137100 polymorphism. Materials and Methods We examined 88 Caucasian girls (aged 15.8±0.09) with body mass index SDS (SDS BMI) ≥2.0, living in Eastern Siberia (Russia). The SDS BMI≥2.0 girls were divided in 2 groups: 41 girls (aged 15.4±0.1) with android obesity (waist measurement 97.3±1.7‰) and 47 girls with gynoid (waist measurement 86.1±15.1‰), (aged 15.5±0.1). We measured circumference and skinfold thickness in following areas: blades, chest, belly, thighs, triceps, and biceps. We investigated metabolism parameters: glucose, insulin, leptin in serum; insulin sensitivity index (HOMA-IR) was calculated. We tested frequency of LEPR rs1137100 polymorphism in girls with android and gynoid obesity. Results Primarily we compared thickness of subcutaneous adipose tissue in girls-carriers of different genotypes in both groups. Girls with android obesity - carriers of AA genotype, thickness of subcutaneous adipose tissue in breast was 1.1±0.2cm; AG genotype - 0.94±0.2cm; GG-genotype - 0.93±0.2cm (pAA-AG; AA-GG=0.04). Metabolism parameters: insulin in carriers of AA genotype was 25.2±13.6; AG genotype - 15.5±8.3; GG genotype –18.1±11.4 (pAA-AG=0.01); HOMA-IR, 6.1±3.6; 3.4±2.0; 4.4±3.3 (pAA-AG=0.01), respectively. Leptin without statistically significant differences was elevated in AA genotype carriers 67.1±25.1, in contrast to carriers of AG and GG genotypes: 54±26.6; 50.8±26.5, respectively. In girls with a gynoid obesity - carriers of AA genotype, thickness of subcutaneous adipose tissue in thighs was 2.0±0.2cm; AG genotype - 2.1±0.3cm; GG-genotype - 2.5±0.8cm (pAA-GG=0.03). Metabolism parameters: insulin in AA genotype carriers was 13.4±5.1; AG genotype - 11.8±6.3; GG genotype - 21±14.2 (pAA-GG=0.04; pAG-GG=0.02). Leptin 34.5±15.7; 32.2±16.3; 55.8±19.7 (pAA-GG=0.005; pAG-GG=0.003) respectively. HOMA-IR in carriers of AA genotype was 3.0±1.6; AG genotype - 2.6±1.4; GG-genotype - 4.5±3.2 (pAG-GG=0.04). Conclusions In girls of android morphotype, the carriage of A-allele is associated with carbohydrate and energy metabolism disorders, and is a risk marker of excess fat deposition in chest area. For a gynoid morphotype, G-allele is a risk marker and is associated with excessive fat deposition in the thighs, as well as with carbohydrate and energy metabolism disorders.