OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) is a multistage disorder that progresses from bland hepatic steatosis, non-alcoholic steatohepatitis, and fibrosis to irreversible cirrhosis. Hyperlipidemia and hyperglycemia, hallmarks of metabolic syndrome suggested being associated with liver dysfunction. The primary aim of this study was to examine the liver function status among adults having both hyperlipidemia and hyperglycemia in the United States. METHODS: The National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2012 was used to examine the association between hyperlipidemia, hyperglycemia and liver enzymes amongst adults in the United States. Data were analyzed for descriptive statistics and for differences using the t test, Chi square test and ANOVA. A regression analysis was performed to identify relationships between demographic and above biomarkers. A p value of < 0.05 was considered statistically significant.   RESULTS: A total of 35,509 adults (≥20 yrs.) were included in this study. Sample mean age was 46.6 ± 0.22 yrs., majority were non-Hispanic white (46.7%) and female (51.3%). Seventy one percent adults had elevated LDL-C (> 130mg/dl), 19% had HDL-C (< 60mg/dl) and 11% had HbA1C > 7%. Adults with combination of hyperlipidemia and hyperglycemia were associated with 42% chance of having elevated ALT, 37% chance of elevated AST and 51% chance of elevated ALP levels. Adults with HbA1C > 7% had 16% chance of elevated ALT, 10% chance of elevated AST and 31% chance of elevated ALP levels (p<0.001). Regression analysis showed significant relationship between age, gender, ethnicity, HbA1C, combination of hyperlipidemia and hyperglycemia, ALT, AST and ALP (p<0.05).    CONCLUSIONS: Chances of having elevated liver enzyme significantly increase when the individual has hyperlipidemia compared to hyperglycemia. Moreover, no potentiation was observed when individuals' had both disease. We hypothesize that augmented levels of blood lipids and glucose indepndantly potentiates the liver dysfunction by initiating inflammatory mediators in the hepatocytes.