Protein levels (Western blot) of the major glucose transporter isoform (GLGT4) were measured in skeletal muscles (quadriceps femoris) of an animal model of human metabolic syndrome X, i.e. the hereditary hypertriglyceridaemic (HTG) insulin-resistant rats fed various diets. The results were compared with the data obtained in normal Wistar rats which underwent the identical protocol. In HTG rats fed the basal diet (B) or high- sucrose diet (HS) (known to induce hypertriglyceridaemia and to impair insulin action), a decrease of GLGT4 protein levels (B: Control 100±3 vs HTG 46±5 %, p<0.005; HS: Control 80±9 vs HTG 49±3 %, p<0.005) was observed. Furthermore, marine Pish oil (FO) rich in n-3 polyunsaturated fatty acids (PGFA), added to the basal diet (30 wt % of n-3 PGFA) reduced the GLGT4 protein levels (B: 100±3 vs B+FO: 42±4 %, p<0.005) in control rats to values similar to those found in HTG rats (B: 46±4 %). However, dietary FO did not have any effect in HTG rats (49±3 %). Feeding the high-sucrose diet supplemented with FO to both the control and HTG rats was followed by a further decrement of GLGT4 protein (Control 15±5 vs HTG 14±4%). In conclusions, a) the hereditary HTG rats had by about 50 % lower GLGT4 protein levels in the quadriceps femoris muscle in comparison to normal Wistar rats; b) high-sucrose diet or raised dietary intake of n-3 PGFA did not further alter the number of glucose carriers in quadriceps femoris muscle in HTG rats and c) feeding the high-sucrose diet with higher proportion of n-3 PGFA was associated with an additional reduction of the GLGT4 protein level in this muscle.