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Bezafibrate, a peroxisome proliferator-activated receptor α agonist, decreases circulating CD14(+)CD16(+) monocytes

Tomoko Terasawa1, Yoshimasa Aso2, Kyoko Omori3

  • 1Department of Internal Medicine, Koshigaya Hospital, Dokkyo Medical University, Koshigaya, Saitama, Japan.

Translational Research : the Journal of Laboratory and Clinical Medicine
|August 20, 2014
PubMed

Insights

Bezafibrate, a PPARα agonist, effectively reduces proinflammatory CD14(+)CD16(+) monocytes in type 2 diabetes patients. This study shows bezafibrate likely inhibits CD16 messenger RNA (mRNA) expression, offering a potential therapeutic strategy for managing diabetes-related inflammation.

Area of Science:

  • Immunology
  • Endocrinology
  • Pharmacology

Background:

  • CD14(+)CD16(+) monocytes are key proinflammatory cells implicated in chronic diseases.
  • Elevated CD14(+)CD16(+) monocyte counts are observed in patients with chronic renal failure and coronary artery disease.
  • These monocytes produce critical inflammatory cytokines such as tumor necrosis factor and interleukin-1β.

Purpose of the Study:

  • To investigate the therapeutic effect of bezafibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist, on circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes.
  • To examine the in vitro impact of bezafibrate on CD16 messenger RNA (mRNA) expression in mononuclear cells (MNCs) from type 2 diabetic subjects.

Main Methods:

  • Cross-sectional and interventional study design involving patients with normal glucose tolerance, impaired glucose tolerance, and type 2 diabetes.
  • Analysis of circulating CD14(+)CD16(+) monocyte percentages using flow cytometry.
  • In vitro experiments assessing CD16 mRNA and IL-1β mRNA expression in MNCs treated with bezafibrate.

Main Results:

  • Subjects with impaired glucose tolerance and type 2 diabetes exhibited significantly higher percentages of CD14(+)CD16(+) monocytes compared to those with normal glucose tolerance.
  • Bezafibrate treatment (400 mg/d) in type 2 diabetes patients led to a significant reduction in circulating CD14(+)CD16(+) monocytes.
  • In vitro studies demonstrated that bezafibrate decreased CD16 mRNA and IL-1β mRNA expression in MNCs, suggesting a molecular mechanism for its anti-inflammatory effects.

Conclusions:

  • Bezafibrate significantly reduces the number of circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes.
  • The observed reduction is likely mediated by the inhibition of CD16 mRNA expression by bezafibrate.
  • These findings suggest that bezafibrate holds potential as a therapeutic agent for mitigating inflammation associated with type 2 diabetes.

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