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Volume 83, Issue 1, Pages 45-54 (July 2010)


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Elevated plasma fibrinogen caused by inadequate α-linolenic acid intake can be reduced by replacing fat with canola-type rapeseed oil

T. Seppänen-Laaksoab, I. LaaksoaCorresponding Author Informationemail address, T. Lehtimäkic, R. Rontuc, E. Moilanend, T. Solakivie, L. Seppofg, H. Vanhanenh, K. Kivirantai, R. Hiltunena

Received 20 December 2008; received in revised form 23 November 2009; accepted 2 February 2010. published online 08 March 2010.

Abstract 

The effects of canola-type rapeseed oil (RSO) on serum lipids, plasma fibrinogen, lipid oxidation and fatty acids were studied in three groups of subjects, two of which had not been consuming fish in their habitual diets. Forty-two volunteers (35 women, 7 men, 16–62 years) replaced fat with RSO for 6 weeks in a parallel design. The average cholesterol and fibrinogen concentrations were 5.0mmol/l and 2.6g/l, respectively. The intake of α-linolenic acid (α-LLA) was doubled. Efficient competitive inhibition by α-LLA was seen as a decrease in long-chain (LC) n-6 PUFA at 3 weeks. Elevated fibrinogen (2.6–3.9g/l) decreased by 0.95g/l at 6 weeks. Docosahexaenoic acid (22:6n-3) in plasma phospholipids increased at low fibrinogen levels only. The associations and changes in plasma C18 and LC PUFA followed the competitive and metabolic principles of the body, and especially in the case of n-3 PUFA according to the recycling pathway.

a Division of Pharmaceutical Biology, Faculty of Pharmacy, University of Helsinki, Finland

b VTT Technical Research Centre of Finland, Espoo, Finland

c Laboratory of Atherosclerosis Genetics, Tampere University Hospital, Centre for Laboratory Medicine, and Department of Clinical Chemistry, Medical School, University of Tampere, Finland

d The Immunopharmacology Research Group, Medical School, University of Tampere, and Research Unit, Tampere University Hospital, Finland

e Department of Medical Biochemistry, Medical School, University of Tampere, Finland

f Foundation for Nutrition Research, Finland

g Institute of Biomedicine, University of Helsinki, Finland

h The Social Insurance Institution of Finland, Helsinki, Finland

i Skin and Allergy Hospital, Helsinki University Central Hospital, Finland

Corresponding Author InformationCorresponding author. Tel.: +358919159185; fax: +358919159138.

 Deceased

PII: S0952-3278(10)00043-8

doi:10.1016/j.plefa.2010.02.001


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