SAT-681 Children With Morbid Obesity And Metabolic Dysfunction-associated Steatotic Liver Disease (masld) Exhibit More Severe Insulin Resistance Compared To Patients With Morbid Obesity Without Masld

Abstract Disclosure: B. Labib: None. L. Musmanno: None. S. Yavuz: None. M. Berra: None. E. Volcotrub: None. M. Gangat: None. A. Khattab: None. I. Marshall: None. P. Rizzuto: None. E. Iofel: None. A.S. Bhangoo: None. S.B. Ten: None. Introduction: Morbid obesity, with significant visceral fat, contributes to increased free fatty acid levels in the blood, which directly impairs insulin signaling in both muscle and liver. Insulin resistance (IR) contributes to the progression of MASLD to metabolic dysfunction-associated steatohepatitis (MASH). Elevated liver function tests (ELFT), specifically ALT and AST at >35 U/L are considered markers for MASLD. The triglyceride to HDL-C ratio (TG/HDL) is considered to be a marker for Insulin Resistance and a surrogate risk marker for cardiovascular disease (CVD). A normal ratio is less than 0.87, while a ratio of more than 2 is associated with a significantly higher risk for metabolic syndrome and CVD.We aimed to evaluate relationships between Insulin Resistance and an increase in liver enzymes levels in patients with morbid obesity. Methodology: IR was calculated using HOMA-IR (Homeostasis Model Assessment of Insulin Resistance), which uses fasting glucose (mg/dL) and fasting insulin (mU/L) levels to estimate IR. The formula for HOMA-IR is fasting glucose (mg/dL) X fasting insulin (mU/L)/405. Optimal HOMA-IR is less than 2.0; mild IR is 2.0-2.9; and moderate to severe IR is more than 3.0. Results: A total of 372 patients (age range 15.8 ± 7.6 yrs; 203 females) with morbid obesity (BMI of 39.5 ± 9.0 kg/m2) were included. Patients were divided into two groups: group 1 (NLFT) with normal ALT and AST, and group 2 (ELFT) with elevated ALT and AST (more than 35 U/L).Group 1: 260 patients (70% of total patients; age range 15.6 ± 7.8 yrs; 159 females) with morbid obesity (BMI of 38.9 ± 9.0 kg/m2), and ALT at 19.8 ± 7.1 U/L, and AST at 20.1 ± 7.6 U/L.HOMA-IR was 6.4 ± 6.1; TG/HDL at 2.9 ± 1.9; TG at 122.8 ± 62.2 mg/dL, HDL-C at 45.6 ± 13.9 mg/dL, LDL-C at 103.5 ± 32.6 mg/dL; HbA1c at 5.5 ± 0.8%; fasting glucose at 92.3 ± 27.5 mg/dL and insulin at 28.4 ± 21.3 µU/mL; leptin at 27 ± 24.8 ng/mL.Group 2: 112 patients (30% of total patients; age range 16.4 ± 6.9 yrs; 44 females) with morbid obesity (BMI of 40.8 ± 8.4 kg/m2), ALT at 89.2 ± 86.2 U/L, and AST at 52.1 ± 45.2 U/L.HOMA-IR was 12.4 ± 6.1; TG/HDL at 4.4 ± 2.4, TG at 173 ± 86.8 mg/dL, HDL-C at 41.5 ± 12 mg/dL, LDL-C at 111.6. ± 33.9 mg/dL; HbA1c at 6.0 ± 1.1%; fasting glucose at 106.9 ± 50.6 mg/dL and insulin at 45.2 ± 34.2 µU/mL; leptin at 23.5 ± 14.5 ng/mL.There were no differences in age, BMI, SBP, DBP, and leptin levels between groups 1 and 2.ALT and AST, HOMA-IR, TG/HDL, TG, LDL-C, HbA1c, fasting glucose, and insulin levels were significantly higher in group 2, p < 0.05. Conclusion: Both groups had IR according to the HOMA-IR and the TG/HDL ratio. The combination of morbid obesity with ELFT leads to a more severe form of IR, increasing the risk of various metabolic complications and CVD. Presentation: Saturday, July 12, 2025