n-3 polyunsaturated fatty acid supplementation, monocyte adhesion moleculeexpression and proinflammatory mediators in Type 2 diabetes mellitus

Citation
Mj. Sampson et al., n-3 polyunsaturated fatty acid supplementation, monocyte adhesion moleculeexpression and proinflammatory mediators in Type 2 diabetes mellitus, DIABET MED, 18(1), 2001, pp. 51-58
Citations number
40
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
DIABETIC MEDICINE
ISSN journal
07423071 → ACNP
Volume
18
Issue
1
Year of publication
2001
Pages
51 - 58
Database
ISI
SICI code
0742-3071(200101)18:1<51:NPFASM>2.0.ZU;2-#
Abstract
Aims To examine the effect of n-3 polyunsaturated fatty acid supplements on the monocyte surface expression of adhesion molecules involved in pro-athe rogenic monocyte-endothelial interactions, and on pro-inflammatory mediator s in Type 2 diabetes mellitus. Methods Twenty-nine subjects with Type 2 diabetes and 21 controls without d iabetes were studied. Monocyte expression of leucocyte function-associated antigens 1 and 3, intercellular adhesion molecule-1, and the major histocom patibility complex class II molecule HLA-DR were measured using a laser flo w cytometric method. Supplementation with 2.08 g n-3 fatty acids for 21 day s was undertaken and measurements repeated. Plasma soluble adhesion molecul e concentrations, plasminogen activator inhibitor-1 activity and antigen an d pro-inflammatory mediators (cysteinyl leukotriene and monocyte leukotrien e B4) were also measured. Results Groups did not differ in monocyte expression of adhesion molecules or HLA-DR, or in leukotriene production although plasma soluble adhesion mo lecule concentrations were higher in the diabetes groups (P < 0.05). n-3 fa tty acid supplementation influenced neither the expression of these molecul es nor plasma soluble adhesion molecule concentrations or leukotriene produ ction. Conclusions This study does not support increased monocyte adhesion molecul e expression or abnormal monocyte production of pro-inflammatory mediators as mechanisms for increased atherogenic risk in Type 2 diabetes. Cardioprot ective actions of n-3 fatty acids may not be mediated through these mechani sms.