Long-term pharmacotherapy in patients with schizophrenia can provoke antipsychotic-induced obesity. This side effect does not always meet the criteria for metabolic syndrome (MS), primarily central obesity. However, this significantly reduces the quality of life of patients and is a risk factor for the development of many diseases. In humans, the NOS1AP gene product is involved in adipogenesis, dendrite maturation, mnemonic processes, and impulse transmission by NMDA receptors. We hypothesized that NOS1AP gene polymorphisms are associated with metabolic parameters in patients with schizophrenia. We examined 491 patients of Slavic nationalities with an established diagnosis of schizophrenia. All participants underwent anthropometric examination to determine waist circumference and the total and visceral fat content using bioimpedance analysis and caliperometry. The biochemical parameters of the blood serum were evaluated by standard methods. MS components were determined according to the International Diabetes Federation criteria. DNA was isolated from peripheral blood leukocytes by the standard phenol-chloroform method. Three SNPs in the NOS1AP gene were selected for genotyping. The alleles of the studied polymorphisms were determined by real-time PCR. As a result, statistically significant differences in the groups of patients with different levels of visceral fat in the distribution of the allele frequency of the s12143842 NOS1AP polymorphism, as well as differences in the levels of visceral fat depending on the rs10494366 NOS1AP genotype were revealed. For the first time, an association of NOS1AP gene polymorphisms with the formation of visceral fat levels in patients with schizophrenia was established. The results obtained can be further used to develop genetic panels to predict the development of adverse metabolic effects during antipsychotic therapy for schizophrenia.