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Objective – to identify different phenotypes of overweight in women with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) based on body mass index (BMI) and serum leptin levels, as well as to determine the frequencies of various metabolic disorders, hypertension and cardiovascular complications in individual phenotypes. Material and methods. The study included 50 women with RA and 46 with SLE aged 18 to 65 years without a history of diabetes and fasting hyperglycemia. The concentration of leptin (ELISA), insulin (electrochemiluminescence analysis) was determined in all patients, and the HOMA-IR index was calculated. Hyperleptinemia was diagnosed at leptin concentrations >11,1 ng/ml, insulin resistance (IR) – at HOMA-IR values ≥2,77. Three main phenotypes of overweight were distinguished: “classic” (BMI≥25 kg/m2 + hyperleptinemia), “healthy” (BMI≥25 kg/m2 , without hyperleptinemia), “hidden” or “latent” (BMI

Objective – to identify obesity/overweight phenotypes in patients with systemic lupus erythematosus (SLE) based on the body mass index (BMI) and serum leptin levels assessment, and to clarify the relationship of these phenotypes with different metabolic disorders.Material and methods. The study included 51 patients with SLE (48 women, 3 men) without diabetes mellitus. The median age of patients was 40 [31; 48] years, disease duration was 3.0 [0.6; 9.0] years. Glucocorticoids were received by 84% of patients, hydroxychloroquine – by 76%, immunosuppressants – by 20%, biological agents – by 10%. BMI was calculated and the fasting leptin level in serum was determined (ELISA) in all patients. Leptin concentrations >11.1 ng/ml in women and >5.6 ng/ml in men corresponded to hyperleptinaemia. There were three main obesity/overweight phenotypes: “classic” (BMI≥25 kg/m2 + hyperleptinemia), “healthy” (BMI≥25 kg/m2 , without hyperleptinemia), “hidden” or “latent” (BMI˂ 25 kg/m2 + hyperleptinemia), as well as “normal weight” (BMI˂ 25 kg/m2 , without hyperleptinemia).Results. The “classic” phenotype of obesity/overweight was diagnosed in 22 (43%) patients, the “healthy” – in 1 (2%), the “hidden” – in 14 (27.5%) patients with SLE. Insulin concentrations were: 10.0 [7.5; 17.9] μU/mL in the “classic” phenotype, 8.3 [6.0; 11.9] μU/mL in the “hidden” phenotype, and 5.3 [4.2; 6.3] μU/ml at “normal weight” (p=0.001). HOMA-IR index were: 2.18 [1.70; 4.23], 1.78 [1.23; 2.41] and 1.18 [0.95; 1.52], respectively (p=0.002). The levels of glucose, total cholesterol, ApoB did not differ in the groups. The uric acid concentrations were the highest in the “classic” phenotype group (334 [365; 388] μmol/l), the lowest in the group of “hidden” obesity/overweight (257 [214; 296] μmol/l), and intermediate in “normal weight” group (286 [236; 377] μmol/l) (p=0.04).Conclusion. The majority of SLE patients hade the “classic” obesity/overweight phenotype, while the “healthy” phenotype was extremely rare. In 27.5% of patients, the presence of a “latent” phenotype was confirmed, which, in terms of metabolic disorders, is an intermediate stage between “normal weight” and “classic” obesity. For rational and timely prevention of insulin resistance, metabolic syndrome and related complications, it is necessary to actively identify the “hidden” phenotype.

Chronic obstructive pulmonary disease (COPD) belongs to urgent medical and social problems of our time. Prognosis of COPD is often determined by a comorbidity, in particular obesity. The key chain, which unites COPD and obesity, is systemic inflammation, in the development of which the hormone of fatty tissue leptin plays an important role. The presence of receptors to leptin in the alveolar and bronchial epithelial cells, in smooth muscle tissue and submucous bronchial membrane allowes to assume that leptin takes pathogenetic part in COPD progression. The aim of our research was to estimate the leptin level in COPD patient and analyze changes of the respiratory function depending on it. Methods. We have been examined 26 patients with exacerbation of COPD (13 male and 13 female, 58 y.o.) and 20 healthy people representative by gender, age and body mass. The level of serum leptin has been defined by the solid phase enzyme linked immunosorbent analysis, lung function – by computed testing. Results and conclusion. With the leptin level increase all of the lung function parameters progressively decreased, most significant - forced vital capacity and peak expiratory flow. Patients with hyperleptinemia had significantly lower measurements of forced expiratory volume in 1 second and vital lungs capacity. Severe degree of both obstructive and restrictive changes has been found more often among patients with hyperleptinemia and leptin level has been associated with the bronchial obstruction severity.

Temporary cessation or restriction of breastfeeding can lead to metabolic disorders in adulthood. However, data on the effect of fasting in the early postnatal period on the functions of the endocrine system in adulthood are rare and contradictory. Approaches for the correction of metabolic and hormonal disorders caused by premature cessation of breastfeeding have not been developed yet. The aim of the work was to study the metabolic and hormonal parameters and changes in the hormonal status of the gonadal and thyroid systems in 10-month-old male rats with interruption of breastfeeding on days P19-P21, as well as to evaluate the restorative effect on them of four weeks of treatment with intranasal insulin (II) administered in the postnatal period (P28-P55) or in adulthood (P183-P210). Lactation interruption has been induced by treatment of lactating females with bromocriptine (10 mg/day/rat, P19-P21). Male rats with temporary cessation of breastfeeding developed characteristic signs of the metabolic syndrome (obesity, dyslipidemia, impaired glucose tolerance, hyperleptinemia), decreased levels of testosterone and thyroid hormones (fT4, tT3) and weakened the synthesis of testosterone and thyroxine, stimulated respectively by GnRH and thyroliberin. This was due to a decrease in the sensitivity of the testes to luteinizing hormone (LH) and the thyroid gland to thyroid-stimulating hormone (TSH). Treatment with II in early ontogenesis reduced body weight and fat, improved lipid profile, sensitivity to insulin, leptin, LH and TSH, restored the levels of testosterone and thyroid hormones and their stimulation by releasing factors. Treatment with II in adulthood normalized the levels of testosterone, thyroid hormones, their stimulation by releasing factors, but had a little effect on metabolic and hormonal parameters. The obtained data point to a wide range of metabolic and hormonal disorders in adult male rats with the "neonatal" model of metabolic syndrome and to the effectiveness of various strategies for their correction using long-term II treatment.