Dyslipidemia and insulin resistance are a consequence of abnormal lipid metabolism and hepatic lipid accumulation in obese individuals. The mechanism of hepatocellular damage and development of NAFLD though unclear, is commonly attributed to the lipotoxicity of high circulating levels of free fatty acid, total cholesterol and other lipid metabolites. These lipid products in turn contribute to mitochondrial dysfunction due to oxidative stress and free radical damage. The current management strategy for NAFLD in children focuses on weight reduction and normalising lipid levels [24, 25].
Many studies have used different modalities to diagnose NAFLD in children as there is no consensus regarding the diagnostic criteria. US technique sensitivity ranges from 60–94% and a specificity of 84–100% in detecting steatosis .Sensitivity and specificity of US increases to 100% and 90% respectively when hepatic steatosis content exceeds 20% .In the present study, NAFLD diagnosis was based on liver steatosis in US and/or more than 2 times the upper limit of gender specific ALT . The 61.7 % prevalence of NAFLD among obese and overweight children in our study is similar to other published studies from India using similar diagnostic modalities [27, 28].
No significant difference in BMI, SBP, DBP and WC between NAFLD and non-NAFLD group were noted. This observation is discordant with findings of many western and Indian studies [27–29]. Pawar et al found that systolic hypertension was the sole independent factor associated with NAFLD . Another study found that BMI, WC, SBP, DBP were significantly higher in NAFLD group among 11–16 year old children .
Though we observed apparent increase of non HDL lipid levels (TC, TG, LDL, VLDL) in NAFLD group, significant statistical difference was found only with LDL. Though some studies demonstrated increased lipid levels like cholesterol, triglycerides in NAFLD patients, the findings are not consistent [27–32]. On similar lines, HDL cholesterol was observed to be lesser in the NAFLD group compared to the non-NAFLD group without statistically significant difference. Pawar et al demonstrated higher triglyceride and AST levels in NAFLD children . Two similar studies also found significant association between low HDL levels and NAFLD [29, 32]. Though many studies have confirmed the association of insulin resistance with NAFLD [8, 28, 29], Pawar et al  found no difference in insulin and HOMA-IR levels between NAFLD and non-NAFLD group which is similar to our study. This finding can be partly explained by the relative younger pre-pubertal age group of the study population compared to adolescent age group in many other studies as the progression of insulin resistance is directly proportional to the increasing age in children. Our study population included children less than 13 years of age whereas many studies included children till 16 to 18 years of age.
Since most patients were asymptomatic except for Obesity and overweight, liver biopsy was not done to evaluate NAFLD. MRI is considered as better imaging modality to confirm NAFLD in children. MRI proton density fat fraction (MRI-PDFF) is superior in classifying grades of steatosis based on a recent meta-analysis in 2019 with pooled sensitivity and specificity of MRI-PDFF for grades 0 vs. 1–3, 0–1 vs. 2–3, and 0–2 vs. 3 were 0.93 and 0.94, 0.74 and 0.90, and 0.74 and 0.87, respectively . Due to practical limitations in a resource limited setup and poor patient affordability, MRI imaging could not be performed to diagnose NAFLD. Other limitations of this study include lack of non-obese controls and not using fibroscan, a specialized ultrasound to assess steatosis and fibrosis of NAFLD. Since more sensitive methods for diagnosis of NAFLD were not used in this study, the results obtained are different and discordant from the published data in literature.