Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Dietary Supplementation with co‐3‐Polyunsaturated Fatty Acids Decreases Mononuclear Cell Proliferation and Interleukin‐1β Content but not Monokine Secretion in Healthy and Insulin‐Dependent Diabetic Individuals

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Changes in the lipidome in type 1 diabetes following low carbohydrate diet: Post-hoc analysis of a randomized crossover trial

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. The Rac2 GTPase contributes to cathepsin H-mediated protection against cytokine-induced apoptosis in insulin-secreting cells

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Characterization of plasma lipidomics in adolescent subjects with increased risk for type 1 diabetes in the DiPiS cohort

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Long Noncoding RNAs in Diabetes and β-Cell Regulation

    Research output: Chapter in Book/Report/Conference proceedingBook chapterResearchpeer-review

  5. Increased levels of inflammatory factors are associated with severity of polyneuropathy in type 1 diabetes

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

The effects of dietary supplementation with ω‐3‐polyunsaturated fatty acids (ω‐3‐PUFA) on the proliferative response of PBMC and on the secretion of monokines and arachidonic acid metabolites from PBMC and monocytes (Mo) from healthy subjects and patients with recent‐onset insulin‐dependent diabetes mellitus (IDDM) were examined. Three groups of eight to nine healthy individuals were randomized to either 2.0 g/day or 4.0 g/day of ω‐3‐PUFA devoid of vitamins A and D, or an isocaloric amount of placebo. Furthermore, eight patients with recent‐onset IDDM received 4.0 g/day of ω‐3‐PUFA. IL‐lβ production and TNF‐α secretion was determined before and after 7 weeks of treatment, and 10 weeks after withdrawal of treatment. Significant increases in platelet and PBMC membrane eicosapentaenoic acid was found in ω‐3‐PUFA‐treated individuals. ω‐3‐PUFA treatment significantly reduced the content of IL‐Ib in lysates of PBMC, but did not affect PBMC or Mo secretion of IL‐1β, TNF‐α or prostaglandin E2 (PGE2) or PBMC leukotriene B4 (LTB4) secretion in healthy subjects or in IDDM patients. A significant inhibition of the PHA‐stimulated. but not the spontaneous or PPD‐stimulated, proliferative response of PBMC was observed in healthy and diabetic subjects treated with (o‐3‐PUFA. No correlation was found between PHA‐stimulated PBMC proliferation and PBMC secretion of TNF‐α and IL‐1β. There were no significant differences in the spontaneous or the PPD‐or PHA‐stimulated proliferative responses of PBMC between diabetic and healthy individuals at entry. We conclude that although dietary supplementation with 4.0 g/day of ω‐3‐PUFA inhibits the proliferation of PBMC and reduces IL‐I immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects.

Original languageEnglish
JournalScandinavian Journal of Immunology
Volume34
Issue number4
Pages (from-to)399-410
Number of pages12
ISSN0300-9475
DOIs
Publication statusPublished - 1 Jan 1991

ID: 56664951