Abstract
Non-alcoholic fatty liver disease (NAFLD) is recognized as a liver manifestation of metabolic syndrome, accompanied with excessive fat accumulation in the liver and other vital organs. Ectopic fat accumulation was previously associated with negative effects at the systemic and local level in the human body. Thus, we aimed to identify and assess the predictive capability of novel potential metabolic biomarkers for ectopic fat depots in non-diabetic men with NAFLD, using the inflammation-associated proteome, lipidome and metabolome. Myocardial and hepatic triglycerides were measured with magnetic spectroscopy while function of left ventricle, pericardial and epicardial fat, subcutaneous and visceral adipose tissue were measured with magnetic resonance imaging. Measured ectopic fat depots were profiled and predicted using a Random Forest algorithm, and by estimating the Area Under the Receiver Operating Characteristic curves. We have identified distinct metabolic signatures of fat depots in the liver (TAG50:1, glutamate, diSM18:0 and CE20:3), pericardium (N-palmitoyl-sphinganine, HGF, diSM18:0, glutamate, and TNFSF14), epicardium (sphingomyelin, CE20:3, PC38:3 and TNFSF14), and myocardium (CE20:3, LAPTGF-β1, glutamate and glucose). Our analyses highlighted non-invasive biomarkers that accurately predict ectopic fat depots, and reflect their distinct metabolic signatures in subjects with NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is recognized as a liver manifestation of metabolic syndrome, accompanied with excessive fat accumulation in the liver and other vital organs
NAFLD is linked to metabolic syndrome (MetS), a cluster of risk factors including central obesity, high blood pressure, elevated level of fasting plasma glucose, high serum triglycerides (TGs) and low levels of high-density lipoproteins (HDL)
Myocardial TG content is higher in subjects with obesity[10], MetS11, impaired glucose tolerance[12] or T2D13,14, suggesting that cardiac steatosis is relatively common in humans
Summary
Non-alcoholic fatty liver disease (NAFLD) is recognized as a liver manifestation of metabolic syndrome, accompanied with excessive fat accumulation in the liver and other vital organs. NAFLD is linked to metabolic syndrome (MetS), a cluster of risk factors including central obesity, high blood pressure, elevated level of fasting plasma glucose, high serum triglycerides (TGs) and low levels of high-density lipoproteins (HDL). These complications are well known causative factors of insulin resistance (IR), type 2. We have previously shown that in obese, non-diabetic men only accumulation of epicardial and pericardial, but not of myocardial TG, was linked to the severity of structural and functional alterations of the heart[18]. We determined the independent role of a broad panel of parameters comprising plasma proteins associated with inflammation as well as plasma lipid (lipidome) and metabolite (metabolome) signatures in the occurrence of myocardial, epicardial, pericardial and liver fat among male subjects with NAFLD
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