The Role of Prostanoids in the Development of Diabetic Embryopathy

Arnon Wiznitzer*, Boris Furman, Moshe Mazor, E. Albert Reece

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

In infants of diabetic mothers, congenital anomalies occur about two-three times as often as in normal population. Many etiologic factors have been proposed regarding the mechanism of diabetes related birth defects. The metabolic alterations associated with hyperglycemia include myo-inositol and arachidonic acid deficiency, and as a result disturbed metabolism of prostaglandins. Recent studies provide evidence that a deficiency in prostaglandins adversely affects membranogenesis and membrane function. These changes in membrane function permit the influx of high levels of glucose into the cells, inducing the generation of free oxygen radicals that cause morphologic damage of the embryo, involving aberrant mitochondrial function and enhanced peroxidation of embryonic lipids. The functional deficiency of prostaglandins at a critical time of fetal development can cause embryonic malformations. This paper reviews the role of prostanoids in the development of diabetic embryopathy.

Original languageEnglish
Pages (from-to)175-182
Number of pages8
JournalSeminars in Reproductive Medicine
Volume17
Issue number2
DOIs
StatePublished - 1999
Externally publishedYes

Keywords

  • Diabetic embryopathy
  • Free oxygen radicals
  • Hyperglycemia
  • Prostanoids

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