Diabetes-induced impairment of macrophage cytokine release in a rat model: Potential role of serum lipids

Deborah L. Doxey, Salvador Nares, Bina Park, Chi Trieu, Christopher W. Cutler, Anthony M. Iacopino

Research output: Contribution to journalArticle

50 Scopus citations

Abstract

Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important cell in the complex process of wound repair representing the major source of cytokines throughout the wound healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It has been suggested that diabetes impairs wound healing through disruption of local cytokine production. We previously demonstrated that platelet-derived growth factor B chain (PDGF-B) levels are deficient at the wound site of diabetic rats. In the present study, we measured the levels of several marker cytokines released from cultured peritoneal macrophages of diabetic, nondiabetic hyperlipidemic, and normal rats. The diabetic condition was associated with a generalized reduction of macrophage cytokine release. Nondiabetic hyperlipidemic animals demonstrated similar cytokine reduction supporting the hypothesis that elevated serum lipids are the primary determinants of diabetes-induced reductions in macrophage cytokine release. Thus, manipulation of serum lipids may be a therapeutically useful modality for controlling macrophage cytokine release in the inflammatory and/or wound environment.

Original languageEnglish (US)
Pages (from-to)1127-1136
Number of pages10
JournalLife sciences
Volume63
Issue number13
DOIs
StatePublished - Aug 21 1998
Externally publishedYes

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Keywords

  • Cytokines
  • Diabetes
  • Fenofibrate
  • Hyperlipidemia
  • Macrophage
  • Rat model

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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