Alterations in serum phosphatidylcholine fatty acyl species by eicosapentaenoic and docosahexaenoic ethyl esters in patients with severe hypertriglyceridemia.
A new and sensitive method has been developed to analyze the molecular species of glycerophospholipids. This method was used to examine the effects of hypolipidemic intervention with n-3 fatty acids on the serum phosphatidylcholine species in severely hypertriglyceridemic patients. The drug treated group (n = 19) received 4 g/day of an 85% concentrate of the ethyl esters of eicosapentenoic and docosahexaenoic acids for 6 weeks. Control patients (n = 21) received 4 g/day of ethyl esters of corn oil fatty acids. To evaluate the effects of n-3 fatty acids upon serum phosphatidylcholines (PCs), sera from treated and control patients were analyzed before and after 6 weeks of intervention. PCs isolated from sera were digested with phospholipase C to diglycerides, derivatized with 7-methoxycoumarin-3-carbonyl azide, and analyzed by reverse phase high performance liquid chromatography (HPLC) with fluorescence detection. Pre-intervention serum PC species were, in order of decreasing concentration C16:0,18:2, C16:0,18:1, C18:0,18:2, C16:0,20:1, C16:0,22:0, C18:0,20:4, C16:0,16:0, C18:0,18:1, C18:1,18:2, C16:0,20:5, and C18:1,20:5. In the treated patients, mean increases of 300% in C16:0,20:5 and of 160% in C16:0,22:6 species were observed. There were no significant changes in the molecular species of the serum phosphatidylcholines in the group receiving the corn oil ethyl esters. The cumulative relative percentages for each of the individual fatty acids measured by HPLC were comparable to those determined by gas-liquid chromatography (GLC). In the treated group plasma triglycerides were reduced 26%, while they were increased by 7% in the placebo group. Our data showed that incorporation of eicosapentaenoic and docosahexaenoic acid into the serum PCs occurred within 6 weeks primarily in the C16:0,20:5 and C16:0,22:6 species and were usually accompanied by a reduction in plasma triglyceride.
McKeone
B J
BJ
Baylor College of Medicine, Houston, TX, USA.
Osmundsen
K
K
Brauchi
D
D
Pao
Q
Q
Payton-Ross
C
C
Kilinç
C
C
Kummerow
F A
FA
Pownall
H J
HJ
D000284:Administration, Oral; D002851:Chromatography, High Pressure Liquid; D004075:Diglycerides / Q000097:blood; D004281:Docosahexaenoic Acids / Q000008:administration & dosage / Q000627:therapeutic use*; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D004952:Esters / Q000627:therapeutic use; D015525:Fatty Acids, Omega-3 / Q000097:blood; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000188:drug therapy*; D010713:Phosphatidylcholines / Q000097:blood* / Q000737:chemistry; D014280:Triglycerides / Q000097:blood; D010738:Type C Phospholipases / Q000378:metabolism
D004075:Diglycerides; D004952:Esters; D015525:Fatty Acids, Omega-3; D010713:Phosphatidylcholines; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D010738:Type C Phospholipases