Low Skeletal Muscle Mass Identifies Very High Metabolic Risk in Slovak Children with Obesity: A Body Composition-Based Approach to Risk Stratification.

Obese children had significantly higher mean HOMA-IR compared to controls despite similar prevalence of HOMA-IR-defined insulin resistance using respective cut-offs.

• Study included 54 obese children (BMI 29.5 ± 4.7 kg/m²) and 33 controls (BMI 20.6 ± 1.9 kg/m²) in a cross-sectional design.
• 44.4% of obese children demonstrated HOMA-IR-defined insulin resistance versus 45.5% of controls using their respective cut-offs (HOMA-IR >3.42 for obese, >1.68 for controls).
• Mean HOMA-IR was significantly higher in obese children: 3.66 ± 2.09 vs. 2.53 ± 2.59 (p = 0.034).
• Age-matched analysis (n = 28 pairs, mean age difference 0.22 years) confirmed these findings: HOMA-IR 3.46 ± 2.18 vs. 2.27 ± 2.22 (p = 0.0271).

The TG/HDL-C ratio identified insulin resistance in a substantially higher proportion of obese children compared to controls.

• TG/HDL-C ratio >0.99 mmol/L was used as the cut-off for insulin resistance.
• 38.9% of obese children met TG/HDL-C criteria for insulin resistance versus 12.1% of controls.
• This marker was used alongside HOMA-IR as a complementary validated metabolic marker.

Concordant elevation of both HOMA-IR and TG/HDL-C markers was significantly more common in obese children than controls.

• 22.2% of obese children showed concordant elevation of both metabolic markers versus 6.1% of controls (OR 4.43).
• In the age-matched analysis, the difference was even more pronounced: 17.9% vs. 3.6%.
• Concordant elevation of both markers was used as an indicator of severe metabolic dysfunction.

A subgroup of obese children characterized by low skeletal muscle mass and high body fat demonstrated extremely high insulin resistance prevalence.

• Low skeletal muscle mass was defined as <25th percentile for age and sex; high body fat was defined as >40%.
• 22.6% of obese children met criteria for this low muscle mass/high fat phenotype.
• This subgroup demonstrated 91.7% insulin resistance prevalence versus 31.0% in obese children without low muscle mass (p < 0.001).
• HOMA-IR was 1.9 points higher in the low muscle mass group (95% CI: 0.31–2.73).

Children with low skeletal muscle mass had a 6-fold increased odds of concordant elevation of both metabolic markers compared to those without low muscle mass.

• 50% of obese children with low muscle mass showed concordant elevation of both HOMA-IR and TG/HDL-C markers.
• Only 14.3% of obese children without low muscle mass showed concordant elevation of both markers.
• The odds ratio for concordant elevation in the low muscle mass group was 6.0.

Age-matched sensitivity analysis confirmed that metabolic differences between obese and control children were independent of age effects.

• Age-matched analysis was performed on 28 pairs with a mean age difference of 0.22 years.
• HOMA-IR remained significantly higher in the obese group in age-matched analysis: 3.46 ± 2.18 vs. 2.27 ± 2.22 (p = 0.0271).
• The difference in concordant marker elevation was more pronounced in age-matched analysis (17.9% vs. 3.6%) than in the full cohort (22.2% vs. 6.1%).

The study employed multiple validated insulin resistance markers alongside bioelectrical impedance analysis for body composition assessment.

• All participants underwent bioelectrical impedance analysis and fasting metabolic profiling.
• Insulin resistance was assessed using both HOMA-IR and TG/HDL-C ratio as complementary markers.
• Separate HOMA-IR cut-offs were applied for obese (>3.42) and control (>1.68) children.
• The study design was cross-sectional with 54 obese children and 33 controls.