The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin

R. C. Block; R. Duff; P. Lawrence; L. Kakinami; J. T. Brenna; G. C. Shearer; N. Meednu; S. Mousa; A. Friedman; W. S. Harris; Mark Larson; S. Georas

doi:10.1016/j.plefa.2009.12.005

The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin

R. C. Block
, R. Duff
, P. Lawrence
, L. Kakinami
, J. T. Brenna
, G. C. Shearer
, N. Meednu
, S. Mousa
, A. Friedman
, W. S. Harris
, Mark Larson
, S. Georas

Research output: Contribution to journal › Article › peer-review

31 Scopus citations

Abstract

Lysophophatidylcholine (LPC) and lysophosphatidic acid (LPA) are potent lysolipid mediators increasingly linked with atherosclerosis and inflammation. A current model proposing that plasma LPA is produced when LPC is hydrolyzed by the enzyme autotaxin has not been rigorously investigated in human subjects. We conducted a clinical trial of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and aspirin ingestion in normal volunteers. Fasting blood samples were drawn at baseline and after 4-week supplementation with EPA/DHA (3.4. g/d) with and without aspirin (650. mg). Plasma LPC and LPA species and autotaxin activity were measured. EPA-LPC and DHA-LPC concentrations increased significantly with EPA/DHA supplementation whereas EPA- and DHA-LPA did not. Autotaxin activity was unaffected by any treatment, and aspirin had no effect on any endpoint. Taken together, our data demonstrate that plasma LPC, but not LPA, species can be dynamically regulated by dietary supplementation, and argue against a simple model of LPA generation via LPC hydrolysis.

Original language	English (US)
Pages (from-to)	87-95
Number of pages	9
Journal	Prostaglandins Leukotrienes and Essential Fatty Acids
Volume	82
Issue number	2-3
DOIs	https://doi.org/10.1016/j.plefa.2009.12.005
State	Published - Feb 2010
Externally published	Yes

Funding

The Novel Clinical and Translational Methodologies funding mechanism within the University of Rochester's NIH Clinical and Translational Science Institute also provided funding for this research. Additional resources were provided by R01 HL071933 (S.G.), Reliant Pharmaceuticals and by NIH Grant (P20 RR016479) from the INBRE Program of the National Center for Research Resources.

Funders	Funder number
Nevada INBRE
Clinical and Translational Science Institute at Children's National Medical Center NIH/NCRR	R01 HL071933
Novel Clinical and Translational Methodologies
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	P20 RR016479
National Institute of Health National Heart, Lung, and Blood Institute	R01HL071933
National Center for Research Resources

Keywords

Autotaxin
Docosahexaenoic acid
Eicosapentaenoic acid
Lysophosphatidic acid
Lysophosphatidylcholine
Lysophospholipase D

ASJC Scopus subject areas

Clinical Biochemistry
Cell Biology

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10.1016/j.plefa.2009.12.005

Cite this

Block, R. C., Duff, R., Lawrence, P., Kakinami, L., Brenna, J. T., Shearer, G. C., Meednu, N., Mousa, S., Friedman, A., Harris, W. S., Larson, M., & Georas, S. (2010). The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin. Prostaglandins Leukotrienes and Essential Fatty Acids, 82(2-3), 87-95. https://doi.org/10.1016/j.plefa.2009.12.005

@article{c6a6bd36c79d4883b0f7178678f9f1bf,

title = "The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin",

abstract = "Lysophophatidylcholine (LPC) and lysophosphatidic acid (LPA) are potent lysolipid mediators increasingly linked with atherosclerosis and inflammation. A current model proposing that plasma LPA is produced when LPC is hydrolyzed by the enzyme autotaxin has not been rigorously investigated in human subjects. We conducted a clinical trial of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and aspirin ingestion in normal volunteers. Fasting blood samples were drawn at baseline and after 4-week supplementation with EPA/DHA (3.4. g/d) with and without aspirin (650. mg). Plasma LPC and LPA species and autotaxin activity were measured. EPA-LPC and DHA-LPC concentrations increased significantly with EPA/DHA supplementation whereas EPA- and DHA-LPA did not. Autotaxin activity was unaffected by any treatment, and aspirin had no effect on any endpoint. Taken together, our data demonstrate that plasma LPC, but not LPA, species can be dynamically regulated by dietary supplementation, and argue against a simple model of LPA generation via LPC hydrolysis.",

keywords = "Autotaxin, Docosahexaenoic acid, Eicosapentaenoic acid, Lysophosphatidic acid, Lysophosphatidylcholine, Lysophospholipase D",

author = "Block, \{R. C.\} and R. Duff and P. Lawrence and L. Kakinami and Brenna, \{J. T.\} and Shearer, \{G. C.\} and N. Meednu and S. Mousa and A. Friedman and Harris, \{W. S.\} and Mark Larson and S. Georas",

note = "Funding Information: The Novel Clinical and Translational Methodologies funding mechanism within the University of Rochester's NIH Clinical and Translational Science Institute also provided funding for this research. Additional resources were provided by R01 HL071933 (S.G.), Reliant Pharmaceuticals and by NIH Grant (P20 RR016479) from the INBRE Program of the National Center for Research Resources. Funding Information: This publication was made possible by Grant Number KL2 RR 024136 from the National Center for Research Resources (NCRR) , a component of the National Institutes of Health (NIH) and the NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/ . ",

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doi = "10.1016/j.plefa.2009.12.005",

language = "English (US)",

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T1 - The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin

AU - Block, R. C.

AU - Duff, R.

AU - Lawrence, P.

AU - Kakinami, L.

AU - Brenna, J. T.

AU - Shearer, G. C.

AU - Meednu, N.

AU - Mousa, S.

AU - Friedman, A.

AU - Harris, W. S.

AU - Larson, Mark

AU - Georas, S.

N1 - Funding Information: The Novel Clinical and Translational Methodologies funding mechanism within the University of Rochester's NIH Clinical and Translational Science Institute also provided funding for this research. Additional resources were provided by R01 HL071933 (S.G.), Reliant Pharmaceuticals and by NIH Grant (P20 RR016479) from the INBRE Program of the National Center for Research Resources. Funding Information: This publication was made possible by Grant Number KL2 RR 024136 from the National Center for Research Resources (NCRR) , a component of the National Institutes of Health (NIH) and the NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/ .

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N2 - Lysophophatidylcholine (LPC) and lysophosphatidic acid (LPA) are potent lysolipid mediators increasingly linked with atherosclerosis and inflammation. A current model proposing that plasma LPA is produced when LPC is hydrolyzed by the enzyme autotaxin has not been rigorously investigated in human subjects. We conducted a clinical trial of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and aspirin ingestion in normal volunteers. Fasting blood samples were drawn at baseline and after 4-week supplementation with EPA/DHA (3.4. g/d) with and without aspirin (650. mg). Plasma LPC and LPA species and autotaxin activity were measured. EPA-LPC and DHA-LPC concentrations increased significantly with EPA/DHA supplementation whereas EPA- and DHA-LPA did not. Autotaxin activity was unaffected by any treatment, and aspirin had no effect on any endpoint. Taken together, our data demonstrate that plasma LPC, but not LPA, species can be dynamically regulated by dietary supplementation, and argue against a simple model of LPA generation via LPC hydrolysis.

AB - Lysophophatidylcholine (LPC) and lysophosphatidic acid (LPA) are potent lysolipid mediators increasingly linked with atherosclerosis and inflammation. A current model proposing that plasma LPA is produced when LPC is hydrolyzed by the enzyme autotaxin has not been rigorously investigated in human subjects. We conducted a clinical trial of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and aspirin ingestion in normal volunteers. Fasting blood samples were drawn at baseline and after 4-week supplementation with EPA/DHA (3.4. g/d) with and without aspirin (650. mg). Plasma LPC and LPA species and autotaxin activity were measured. EPA-LPC and DHA-LPC concentrations increased significantly with EPA/DHA supplementation whereas EPA- and DHA-LPA did not. Autotaxin activity was unaffected by any treatment, and aspirin had no effect on any endpoint. Taken together, our data demonstrate that plasma LPC, but not LPA, species can be dynamically regulated by dietary supplementation, and argue against a simple model of LPA generation via LPC hydrolysis.

KW - Autotaxin

KW - Docosahexaenoic acid

KW - Eicosapentaenoic acid

KW - Lysophosphatidic acid

KW - Lysophosphatidylcholine

KW - Lysophospholipase D

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ER -

The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin

Abstract

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Keywords

ASJC Scopus subject areas

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