It was previously found that when it is treated type 2 diabetes mellitus (DM2) by metformin, hyperlactemia does not develop or occurs extremely rarely, and due to concomitant pathology. Clinicians usually do not monitor blood lactate levels. Goal: to analyze the frequency of hyperlactatemia in patients with DM2, its possible causes and role in this of metformin, clinical manifestations, ways of elimination and prevention. We observed in the dynamics of 38 patients with DM2 receiving metformin in doses of 1500–3000 mg / day. All patients were tested the level of lactate in the blood. Hyperlactatemia was detected in 6 cases (12.8% of patients), of which two patients (5.3%) showed lactic acidosis: the blood lactate level of them was 4.0 μmol/L and 4.6 μmol/L. A correlation between the level of lactic acid and the dose of metformin has not been established. All observed patients had polymorbidity and compelled polypharmacy. Hypothyroidism was observed in 42.1% of patients; in patients with lactic acidosis hypothyroidism was decompensated, i.e. it was chronic oxygen starvation of tissues. Conclusion: Observations confirmed that treatment of DM2 with metformin is rarely complicated by lactic acidosis and even moderate hyperlactatemia. Complications of diabetes, concomitant pathology and compelled polypharmacy, including metformin, disrupt the metabolism of lactic acid, its elimination, utilization in gluconeogenesis processes; in ≈12.8% of cases, the level of lactate in the blood rises. The risk of lactic acidosis, i.e. death threat occurs in ≈5.3% of patients. Along with the etiological factors of lactic acidosis widely presented in publications in patients with type 2 diabetes mellitus, in ≈42.1% of cases, lactate accumulation is promoted by hypothyroidism, the decompensation of which creates chronic oxygen starvation of tissues. To check periodically the level of lactic acid and monitor the function of the thyroid gland it is necessary in all patients with DM2, even if they are not treated with metformin.