The first primary research objective of the study is to determine whether high-fat load (150 g of fat) induces increase in hepatic fat content (HFC) three and six hours after meal in insulin-sensitive subjects with normal HFC (<5% of fat) and in non-diabetic subjects with an increased HFC (>5% of fat). Furthermore, the other objective of the study is to determine whether the response of HFC to a high-fat load is affected by coadministration of glucose or fructose.

The epidemic of non-alcoholic fatty liver disease (NAFLD) is becoming a major challenge faced by health system worldwide. The hepatic fat comes from the major sources - non-esterified fatty acids (NEFA) released from adipose tissue, dietary fat and de novo lipogenesis. Fat accumulation in the liver then occurs when triglycerides (TG) that are formed are not rapidly enough oxidized or secreted from the liver in very low density lipoproteins (VLDL). It can be hypothesized that the capacity of the liver to eliminate TG can be overcome after high load of dietary fat. High-fat load should induce an immediate accumulation of hepatic fat that could be detected using 1H magnetic resonance spectroscopy (1H-MRS). The accumulation of liver fat can be also affected by coadministration of simple carbohydrates - glucose and fructose. The administration of these carbohydrates can have a pronounced impact on the availability of particular sources of hepatic fat.

Inclusion Criteria:

• normal response to oral glucose tolerance test
• normal glycated hemoglobin
• normal aspartate aminotransferase (AST)
• normal alanine aminotransferase (ALT)

Exclusion Criteria:

• BMI > 30 kg/m2
• use of pharmacological agents affecting insulin sensitivity
• use of pharmacological agents affecting lipid metabolism
• inability to undergo 1H-MRS examination