Dietary supplementation with omega-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1 beta content but not monokine secretion in healthy and insulin-dependent diabetic individuals

Scand J Immunol. 1991 Oct;34(4):399-410. doi: 10.1111/j.1365-3083.1991.tb01563.x.

Abstract

The effects of dietary supplementation with omega-3-polyunsaturated fatty acids (omega-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 omega-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 omega-3-PUFA. IL-1 beta production and TNF-alpha 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 omega-3-PUFA-treated individuals. omega-3-PUFA treatment significantly reduced the content of IL-1 beta in lysates of PBMC, but did not affect PBMC or Mo secretion of IL-1 beta, TNF-alpha 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 omega-3-PUFA. No correlation was found between PHA-stimulated PBMC proliferation and PBMC secretion of TNF-alpha and IL-1 beta. 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 omega-3-PUFA inhibits the proliferation of PBMC and reduces IL-1 beta immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects.

Publication types

  • Clinical Trial
  • Comparative Study
  • Randomized Controlled Trial

MeSH terms

  • Adult
  • Blood Glucose / analysis
  • Blood Sedimentation / drug effects
  • Cell Division / drug effects
  • Diabetes Mellitus, Type 1 / diet therapy*
  • Diabetes Mellitus, Type 1 / drug therapy*
  • Diabetes Mellitus, Type 1 / metabolism
  • Diabetes Mellitus, Type 1 / pathology
  • Dinoprostone / metabolism
  • Dose-Response Relationship, Drug
  • Fatty Acids, Unsaturated / pharmacology*
  • Humans
  • Interleukin-1 / biosynthesis*
  • Leukocyte Count
  • Leukocytes, Mononuclear / cytology
  • Leukocytes, Mononuclear / drug effects*
  • Leukocytes, Mononuclear / metabolism
  • Leukotriene B4 / metabolism
  • Lipopolysaccharides
  • Male
  • Monocytes / cytology
  • Monocytes / drug effects
  • Monocytes / metabolism
  • Monokines / metabolism*
  • Phenylenediamines
  • Phytohemagglutinins
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Blood Glucose
  • Fatty Acids, Unsaturated
  • Interleukin-1
  • Lipopolysaccharides
  • Monokines
  • Phenylenediamines
  • Phytohemagglutinins
  • Tumor Necrosis Factor-alpha
  • Leukotriene B4
  • Dinoprostone