The absence of clear diagnostic criteria, specific biomarkers, and the heterogeneity of asthma-COPD overlap (ACO) pose challenges in studying both the epidemiology and molecular mechanisms of ACO. This leads clinicians to resort to trial and error methods in finding the optimal treatment for ACO patients. Objective: to investigate the clinical and laboratory characteristics in patients with a combined course of ACO and type 2 diabetes mellitus (T2DM). Object and research methods. A total of 120 patients were examined, comprising 22 patients with chronic obstructive pulmonary disease (COPD) (group 1), 21 with asthma (group 2), 24 with ACO (group 3), 31 with ACO+T2DM (group 4), 22 with T2DM (group 5), and 20 healthy individuals (HI) (group 6). The study assessed indicators of pulmonary function test, body mass index, and visceral fat level. Glucose, 8-isoprostane, insulin, sCD14, C-reactive protein, fibrinogen, cholesterol, triglycerides, high-density lipoproteins, low-density lipoproteins, HOMA-IR, QUICKI, TYG indices were examined. Simultaneously, neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio, and systemic immune inflammation index (SIII) were determined. Results. In patients with ACO+T2DM, more pronounced breathlessness on the mMRC scale, increased exacerbation frequency, higher body mass index, visceral fat, and BODE index were observed with the lowest forced expiratory volume in 1st second. Simultaneously, this group of patients exhibited more pronounced dyslipidemia, characterized by higher levels of total cholesterol and triglycerides, along with lower levels of high-density lipoproteins. It was established that the NLR in patients with COPD, asthma and ACO was significantly higher than in patients with T2DM and HI (p<0.05). The median NLR in ACO+T2DM was likely higher compared to the 1st and 2nd groups by 1.32 and 1.38 times, respectively (p<0.05), but did not differ from the 3rd group (p>0.05). Monocyte-lymphocyte ratio allowed differentiation of patients with ACO and ACO+T2DM from the 5th and 6th groups (p<0.05). In all patient groups, the SIII was higher than in HI, and in patients with ACO+T2DM, this index was higher than in COPD by 26% (p<0.05) and in T2DM by 25% (p<0.05). The level of 8-isoprostane was highest in ACO+T2DM patients, with a statistically significant difference from all groups, particularly by 62.5; 60 and 41.1% compared to COPD, asthma and ACO, respectively (p<0.05). The level of C-reactive protein was noticeably higher in the main group, with a significant difference between the 5th and 6th groups (p<0.05) and a tendency to higher levels than in asthma. The fibrinogen level in ACO+T2DM patients was 29% higher than in patients with asthma and ACO. In patients with ACO and ACO+T2DM, the sCD14 level was 2.5 times higher than in HI and patients with T2DM (p<0.05), higher than in COPD but slightly lower than in asthma (p>0.05). There was no statistically significant difference between T2DM and HI (p>0.05).