Effects of a Supplementation of n-3 Polyunsaturated Fatty Acids with or without Fish Gelatin on Gene Expression in Peripheral Blood Mononuclear Cells in Obese, Insulin-Resistant SubjectsRudkowska I.a · Ponton A.b · Jacques H.a, c · Lavigne C.a, d · Holub B.J.e · Marette A.a, d · Vohl M.-C.a, c, f
aInstitute of Nutraceuticals and Functional Foods (INAF), Laval University, Quebec, Qué., bMcGill University and Génome Québec Innovation Centre, Montreal, Qué., cDepartment of Food Science and Nutrition, and dQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, Qué., eDepartment of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ont., and fLaboratory of Endocrinology and Genomics, Laval University Hospital Research Center, Quebec, Qué., Canada
Do you have an account?
- Rent for 48h to view
- Buy Cloud Access for unlimited viewing via different devices
- Synchronizing in the ReadCube Cloud
- Printing and saving restrictions apply
Rental: USD 8.50
Cloud: USD 20.00
Article / Publication Details
Aim: To investigate gene expression changes in peripheral blood mononuclear cells (PBMCs) following an n-3 polyunsaturated fatty acid (PUFA) and n-3 PUFA plus fish gelatin (+FG) supplementation. Methods: A transcriptome comparison of 8-week supplementation with n-3 PUFA and n-3 PUFA+FG was carried out in PBMCs of 16 obese insulin-resistant subjects. Results: Erythrocyte n-3 PUFA concentration increased and plasma triglycerides decreased significantly without altering inflammatory parameters after both supplementations. n-3 PUFA supplementation changed the expression of 805 genes, whereas n-3 PUFA+FG supplementation altered the expression of 184 genes. Three genes were commonly changed: fatty acid desaturase 1, free fatty acid receptor 3, and ectodysplasin. Pathway analyses indicate changes in gene expression via the nuclear receptor peroxisome proliferator-activated receptor α pathway after both supplementations. Further, the extent of modifications in the expression of genes implicated in the inflammatory pathways – the oxidative stress response mediated by nuclear factor (erythroid-derived 2)-like 2, nuclear transcription factor ĸB, oxidative stress, and hypoxia-inducible factor signaling – was different after each supplementation. Conclusion: Although n-3 PUFA and n-3 PUFA+FG supplementations have a distinct impact on gene expression levels, the consequences on biochemical parameters and metabolic pathways were comparable after both supplementations.
© 2011 S. Karger AG, Basel
Article / Publication Details
Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.