Background: Liver steatosis (LS) is diagnosed in obesity at very early ages, not exclusively related to overweight severity.
Objective and hypotheses: To investigate the features of patients diagnosed with obesity associated LS (ultrasonography).
Method: We retrospectively studied 88 obese (BMI>+2 SDS) children with LS (LS-OB) and 88 age, gender, race and puberty matched obese children without LS (no-LS-OB). BMI-SDS, body composition (DXA) and abdominal fat distribution (MRI; n=27 in LS-OB), baseline and after OGTT glucose, insulin and derived indexes (HOMA, WBISI), HbA1c, lipid profile, apoprotein-A1 and B, liver enzymes, and uric acid were studied.
Results: LS was mainly diffuse (97.7%) and mild (65.9%). In LS-OB mean age was 12.07±2.81 years and BMI 4.60±2.81 SDS, with 71.6% males/29.4% females (61.2% pubertal) and 56.5% Caucasian and 41.2% Hispanic. LS-OB showed higher AST/ALT (P<0.001), insulin/HOMA (P<0.05) and triglycerides/VLDL (P<0.01) than no-LS-OB; with an IR prevalence of 65.8%, mean HOMA 4.62 and HbA1c >5.7% in 35.9% LS-OB. LS-OB with moderate-severe LS (31.8%) had lower WBISI/HDL (P<0.05), higher AST (P<0.05), ALT (P<0.01), apoprotein-B (P<0.05) and LDL/HDL-ratio (P<0.05) than LS-OB with mild LS; showing higher trunk/lower-limb fat-ratio (trunk/LL, DXA) and visceral/subcutaneous abdominal fat-ratio (Vis/Sq, MRI) (P<0.05). Serum liver enzymes were increased in 40.5% LS-OB, with lower levels in females vs males and prepubertal children vs adolescents (P<0.05). These patients had higher glucose and insulin at 30 min in the OGTT (P<0.05 and P<0.01), cholesterol, apoprotein-B, cholesterol/HDL and LDL/HDL-ratios (P<0.05) and higher trunk/LL and Vis/Sq ratios (P<0.05). Over 30% LS-OB had dyslipidemia (mainly decreased HDL and increased VLDL) and 79.4% low vitamin D (<20 ng/ml), both alterations were more severe in Hispanics (P<0.05), as was acanthosis nigricans (P<0.01).
Conclusion: LS in obese children courses with enhanced insulin resistance and dyslipidemia. Severe OB-LS is associated with greater visceral adiposity and metabolic impairment, which are also influenced by race, sex and pubertal stage.
Funding: This work was supported by the CIBER Fisiopatología de la Obesidad y Nutrición (CB06/03) and the Instituto de Salud Carlos III, Fondo de Investigación Sanitaria (FIS: grant number PI10/00747 and PI13/02195).
01 - 03 Oct 2015
European Society for Paediatric Endocrinology