Obesity is the most common reason for the insulin resistance (IR) though obesity in children is not always associated with IR. The markers based on fasting glucose and/or insulin levels and alternative parameters with conventional lipid-based indexes are used in assessing the IR in clinical practice. The purpose of the research was to assess the relationship between alternative IR surrogate biomarkers as follows: triglycerides (TG) to high-density lipoprotein cholesterol (HDL-C), TG/HDL-C ratio; single-point insulin sensitivity estimator (SPISE) index; triglyceride-glucose index (TyG), with generally accepted indices based on the insulin/glucose ratios, such as HOMA-IR, QUICKI, Caro, in a cohort of obese children and adolescents. Materials and methods used: a single-stage multicenter comparative study was conducted involving 127 patients aged 6 to 17 y/o with simple obesity of varying degrees. The following indices were calculated: HOMA-IR = fasting insulin (mU/ml) x fasting plasma glucose (FPG) (mmol/L) / 22.5; QUICKI = 1/Log (Fasting Insulin, µU/ml) + Log (Fasting Glucose, mg/dl); Caro = fasting plasma glucose (mmol/l) / fasting insulin (μU/ml); TG/HDL-C = TG (mmol/L) / HDL-C (mmol/L); triglyceride-glucose index TyG = Ln [fasting TG (mg/dl) x fasting plasma glucose (mg/dl)/2], where Ln is the logarithm; SPISE = 600 × HDL-C0.185/(TG0.2 x BMI1.338). Results: 75 (59%) boys and 52 (41%) girls were included in the study; the median age was 12.9 [10.4; 14.9] y/o. Pre-pubertal development was recorded in 25 (19.7%), pubertal - in 102 (80.3%). The prevalence of impaired glucose tolerance (IGT) was 5.5%. In children with IGT, the SPISE index was lower than in children with normal glucose tolerance (3.69 [3.49; 4.37] vs. 4.8 [3.99; 5.55], p=0.021) with no statistically significant differences between these groups in other markers. In the IGT subgroup, a high negative correlation was found between SDS BMI and SPISE (R=-0.97). In the general SDS group, BMI correlated with insulin (R=+0.24), TG (R=+0.2), HOMA (R=+0.24), Caro (R=-0.26), TG/HDL-C (R=+0.28) and SPISE (R=-0.65). The SPISE index was lower in girls than in boys (4.94 [3.63; 5.73] vs. 4.07 [3.59; 5.16], p = 0.045). No statistically significant differences were recorded for other gender-related markers. A negative correlation was also found between the obesity degree and SPISE in the subgroups of girls (R=-0.49) and boys (R=-0.70) as well as among pre-pubertal children of both genders (R=-0.61). The maximum correlation between SDS BMI and SPISE was recorded in the subgroup of teenagers of both genders (R=-0.88). In the general group, TyG was weakly correlated with HOMA-IR (R=+0.26) and QUICKI (R=-0.24), while SPISE showed a weak association with all studied insulin indices; no statistically significant correlation between insulin indices and TG/HDL-C was found. In the subgroup of girls, no significant relationships between the evaluated markers were found, in the subgroup of boys, TyG weakly correlated with HOMA-IR (R=+0.29) and QUICKI (R=-0.32). Stronger correlations were recorded in boys between SPISE and all studied insulin indices. In the subgroup of prepubertal patients, a correlation was found between TyG and QUICKI (R=-0.44), SPISE and Caro (R=+0.56), SPISE and HOMA-IR (R=-0.50). The TG/HDL-C ratio did not statistically significantly correlate with traditional IR markers. TyG showed weak correlations with HOMA-IR and QUICKI in the general group and the boys’ subgroup. In the prepubertal period, TyG only weakly correlated with QUICKI and did not show strong associations with insulin-based indices in pubertal children. The SPISE index showed correlations with insulin markers both in the main group and in individual subgroups. Conclusion: the SPISE index can be considered as a relatively simple and accessible method for assessing IR in obese children and adolescents.