Obesity has been a global health problem over the past decades. The search for new ways in the fight against overweight and obesity leads to a deeper understanding of the pathogenetic mechanisms underlying this condition, and with each new study, the understanding of the problem expands first of all from the immunological approach. Despite the active study of the WNT signaling system in recent years, the available literature contains a small number of studies devoted to determining the components of this signaling pathway in the blood serum of obese people, and virtually no studies on WIF-1 and DVL-1. Purpose of the work: to study DVL-1 and WIF-1 in the blood serum of overweight and obese individuals. Patients (n = 210, aged 19 to 65) were examined, divided into 4 groups: I – people with normal body weight, II – patients with excess body weight; III – patients with metabolically healthy obesity, and IV – patients with metabolically unhealthy obesity using general clinical and immunological research methods. The study obtained data on the concentrations of DVL-1 and WIF-1 in the blood serum of patients with overweight, metabolically healthy and unhealthy obesity, and described the correlation between these proteins of the WNT-signaling pathway and clinical and laboratory parameters. In obese patients, statistically significant changes in the values of the components of the WNT signaling system in the blood serum were detected: an increase in the level of DVL-1, as well as an increase in the level of WIF-1 with an increase in the degree of obesity in metabolically healthy individuals. Correlations between DVL-1 and lipid spectrum indicators; between WIF- 1 with cholesterol profile, leukocytes and erythrocyte sedimentation rate were revealed. The pathogenesis of obesity is a complex process in which various immunopathological mechanisms, where the WNT signaling pathway plays one of the leading roles. Although some of the effects mediated by DVL-1 and WIF-1 have recently been elucidated, the details of their integration are a missing link that must be further explored for better understanding of the immunopathogenesis of metainflammation in obesity.