AbstractPurpose of review
The pathophysiologies of nonalcoholic fatty liver disease (NAFLD), metabolic syndrome, and cardiovascular disease are closely interlinked and associated with atherogenic dyslipidemia. Liver and cardiovascular disease may silently progress to advanced stages if alarming signs, such as abdominal obesity, elevated fasting and postprandial triglycerides, and low HDL cholesterol are overlooked. We review the metabolic mechanisms in NAFLD at the cellular level in the context of standard clinical lipid measurements.Recent findings
We discuss the pathogenesis of NAFLD, nonalcoholic steatohepatitis (NASH), and metabolic syndrome, atherogenic dyslipidemia, lipotoxicity, and lipophagy.Summary
Physicians should infer from biomarkers or clinical findings that their abdominally obese patients are at risk of severe cardiovascular, liver fatty disease, or both. Physicians should carry out laboratory tests of plasma cholesterol, triglycerides, LDL and HDL cholesterol, non-HDL cholesterol, apolipoprotein B and platelets, and for diabetes, but importantly, plasma triglycerides also in the nonfasting state. But note, clinical routine plasma lipid and lipoprotein measurements are not necessarily reliable for interpreting severe metabolic changes. Notably, in advanced stages of NAFLD (i.e., late steatohepatitis and cirrhosis), routine lipid profiles do not necessarily show any more abnormalities.