The aim of the study was to perform isomeric analysis of hydroxyeicosatetraenoic
acid (
HETE) in blood samples from obese patients with non-alcoholic (NASH) and alcoholic (ASH)
steatohepatitis. Sixty nine obese patients with
liver steatosis according to abdominal US data and chronic ALT elevation were assign into two groups aecoriing to the evaluation of alcohol consumption by GAGE and AUDIT questionnaires: NASH - 39 patients and ASH - 30 patients. The identification and quantification of 5(S)-hydroxyeicosatetraenoic
acid (5-HETE),
15-HETE and also non-enzymatic oxidation product
11-HETE in blood plasma were carried out by HPLC-MS-TOF with using 2-hydroxyoctanoic
acid as internal standard. The position of
hydroxyl group in
HETE was elucidated by HPLC-MS/MS. The MS/MS transitions were for
15-HETE m/z 319 ---> m/z 219; for
11-HETE m/z 319 --> m/z 167; for5-HETE m/z 319 --> m/z 115. Patients' body composition was evaluated by bioelectrical impedance, resting energy expenditures (REE) were assessed by indirect calorimetry and nutrition pattern was examined by foodfrequency questionnaire. Mean age, BMI and ALT serum level were similar in patients from ASH and NASH groups. Blood plasma 8+12-
HETE concentration was also similar in both groups of patients, but concentration of
15-HETE (21,6±20,2 vs 11,9±13,7µg/ml, p =0,02) and
11-HETE (20,8±21,3 vs 11,2+12,9 ug/ml, p =0,03) was significantly higher in NASH patients. ASHpatients demonstrated higher lean body mass (68,1±10,6 vs 57,9±9,8 kg, p<0,001) and muscle mass (39,3±6,1 vs 33,2±6,8 kg, p<0,04) and higher rate of
protein oxidation (98,5±3 1 vs 76,2±21,1 g/day, p= 0,02) recalculated from REE. There were no differences found in blood
lipids content as well as in consumption of total
dietary fat, however, there was a trend to difference in saturated/
unsaturated fatty acids ratio between groups (2,3±0,2.in NASH and 1,4±0,3 in ASH patients). In conclusion, the rate of production of eicosatetraenoic
acid metabolites by
lipoxygenase pathway is different in NASH and ASH
overweight patients. It means that possibly different mechanisms are responsible for formation of potentially toxic
fatty acids metabolites in these two types of patients. It seems likely that differences in
fatty acids consumption pattern are related to this metabolic pathway.