The aim: to evaluate serum nesfatin-1 levels and their correlation with lipid profile parameters in patients with ischemic heart failure (HF) with and without concomitant metabolic comorbidities such as type 2 diabetes mellitus (T2DM) and obesity.

Materials and methods. The study included 225 patients with HF due to ischemic heart disease, divided into four groups: Group 1 (n = 75) – with T2DM and obesity; Group 2 (n = 50) – with T2DM; Group 3 (n = 50) – with obesity; Group 4 (n = 50) – without metabolic disturbances. Serum nesfatin-1 levels were determined using an enzyme-linked immunosorbent assay (ELISA). Biochemical analysis included measurements of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein cholesterol (VLDL-C), as well as calculation of the atherogenic coefficient (AC). Correlation analysis was performed using Spearman’s rank correlation test.

Results. In patient groups with concomitant metabolic comorbidities (Groups 1, 2, and 3), statistically significant inverse correlations were observed between serum nesfatin-1 levels and pro-atherogenic lipids (TC, TG, LDL-C, VLDL-C), along with a significant direct correlation with the anti-atherogenic fraction (HDL-C). In these groups, higher nesfatin-1 levels were associated with a significant decrease in TC (17.6–24.6 %), TG (11.3–49.6 %), LDL-C (29.1–65.0 %), and AC (49.7–59.6 %), alongside an increase in HDL-C (23.1–44.7 %). In contrast, in Group 4 (patients without metabolic disturbances), the effect of nesfatin-1 on the lipid profile was less pronounced. While TG levels decreased significantly (by 28.6 %), other parameters (TC, HDL-C, LDL-C, AC) showed no statistically significant changes or only minimal variations. These findings suggest a context-dependent role of nesfatin-1 in lipid metabolism, with more pronounced effects in the presence of metabolic comorbidities.

Conclusions. Elevated serum nesfatin-1 levels are associated with an improved lipid profile in patients with ischemic HF complicated by type 2 diabetes mellitus and/or obesity, suggesting a potential protective role of this peptide in the presence of metabolic comorbidities. In contrast, in patients without metabolic disturbances, this effect is markedly attenuated or absent. These findings underscore the need for further investigation into the underlying mechanisms of nesfatin-1 action across different clinical populations.