Експериментальна та клінічна фізіологія і біохіміяIntroduction. The problem of pathological gestational weight gain (GWG) is very topical in terms of prediction of obstetric and perinatal complications. The purpose. This scientific research is aimed to study the association of leptin receptor gene Gln223Arg polymorphism with GWG in the group of pregnant women of reproductive age, with normal pregnancy body mass index, single-pregnancy, same population and race and without severe chronic diseases. Materials and methods. 97 women were involved in the study who visited antenatal clinics in Ivano-Frankivsk, Ukraine during 2016-2018. Patients under 18 years old, those who were diagnosed with multiple pregnancy, severe chronic diseases, overweight, obesity and diabetes mellitus were excluded from the study. The average age of patients was 26.8 ± 2.6 years (95% Cl: 26.3-27.3). The pregnancy weight was 55.8 ± 5.8 kg, BMI 20.6 ± 1.6 kg/m2. The recommended GWG was diagnosed in 33 women (34.0 ± 4.8 %), the insufficient one in 19 cases (19.6 ± 4.0 %) and the excessive - in 45 patients (46.4 ± 5.1 %), according to the recommendations of the Institute of Medicine (IOM) in the USA (2009) and the Order of the Ministry of Health of Ukraine No 417 (2011). The anthropometry was performed as well as the determination of GWG, the measurement of serum leptin concentration was done by the method of immunoassay analysis ELISA at the first and third trimesters of pregnancy. LEPR Gln223Arg polymorphism was determined by a molecular genetic study. "Statistica 6.0" and statistical analysis package ‘Microsoft Excel" were used. Results. 20 patients (20.6 ± 4.1 %) were with the AA genotype, 49 (50.5 ± 5.1%) – with the AG genotype and 28 (28.9 ± 4.6 %) – with the GG genotype. It has been found out statistically that GWG is 1.7 times significantly higher in women with LEPR GG polymorphism than the АА genotype (χ2 = 4.00, р < 0,05). The AA genotype is associated with the decrease of the risk of pathological weight gain during the pregnancy in 5 times: [OR = 0.2 (95% CI: 0.1-0.8), р < 0.05]. The frequency of GG-genotype patients in the group with the excessive GWG in 3 times [OR = 3.0 (95% CI: 1.1-9.1), р < 0.05] is higher as compared to patients with the normal weight gain. Thus, the inheritance of pathological G-homozygotes increases the risk of the excessive GWG in 7 times [OR = 7.5 (95% CI: 2.3-24.5), р < 0.001], as compared to patients with the AA genotype. The strong positive correlation was found between the elevated levels of serum leptin concentration and the GWG in the third trimester (r = 0.65, р = 0.0001). The significant increase in serum leptin concentration was discovered at the end of pregnancy in the patients with the GG genotype as compared to patients with the AA genotype (р < 0.05). In the group with the excessive GWG, the presence of GG-alleles of the LEPR gene is accompanied by a higher level of hyperleptinemia as compared to patients with the AA-genopyte (р < 0.05). Conclusions. The modified transcriptional activity of LEPR gene, associated with lipid and carbohydrate metabolism, has a direct effect on the weight gain during the pregnancy. The results suggested that the modified transcriptional activity of LEPR gene, associated with lipid and carbohydrate metabolism and serum leptin levels predicts the risk of the excessive GWG. It can be assumed that the basis of the excessive hyperleptinemia in pregnant women with the GG genotype polymorphism is placental leptin resistance, which is due to the decrease of leptin receptors regulation. The development of leptin resistance in these patients leads to the decrease of glucose absorption of tissues, the lipid oxidation, signals to the increase of the consumption of food, which leads to the excessive GWG during the pregnancy which can serve as a marker for the maternal genotype and genetic predisposition to the development of metabolic diseases after delivery. Further studies with larger sample size are suggested.
Recieved: 22.05.2019
Ключові слова: gestational weight gain, LEPR Gln223Arg polymorphism, leptin
Повний текст: PDF (Eng)