Journal of the Society for Gynecologic Investigation

 

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Journal of the Society for Gynecologic Investigation, Vol. 1, No. 1, 3-13 (1994)
DOI: 10.1177/107155769400100103


Reviews

Review Article : The Yolk Sac Theory

Closing the Circle on Why Diabetes-Associated Malformations Occur

E. Albert Reece

Departments of Obstetrics and Gynecology, Temple University School of Medicine, Philadelphia, Pennsylvania Yale University School of Medicine, New Haven, Connecticut

Emese Pinter

Departments of Obstetrics and Gynecology, Temple University School of Medicine, Philadelphia, Pennsylvania Yale University School of Medicine, New Haven, Connecticut

Carol Homko

Departments of Obstetrics and Gynecology, Temple University School of Medicine, Philadelphia, Pennsylvania Yale University School of Medicine, New Haven, Connecticut

Ying-King Wu

Departments of Obstetrics and Gynecology, Temple University School of Medicine, Philadelphia, Pennsylvania Yale University School of Medicine, New Haven, Connecticut

Frederick Naftolin

Departments of Obstetrics and Gynecology, Temple University School of Medicine, Philadelphia, Pennsylvania Yale University School of Medicine, New Haven, Connecticut

OBJECTIVE: The purpose of this article is to examine the role of yolk sac failure during organogenesis in the development of diabetes-associated embryopathy.

METHODS: The current literature regarding congenital malformations in diabetic pregnancies was reviewed to elucidate the precise role of the yolk sac in embryonic development and the relation between yolk sac injury and embryopathy.

RESULTS: We and others have demonstrated that hyperglycemia produces a teratogenic effect during organogenesis. In addition, we have shown that the yolk sac appears to be the target site of injury induced by hyperglycemia. We have also presented evidence that cell membrane dysfunc tion leads to failed vitelline vessel formation and that arachidonic acid supplementation prevents many of the morphologic and biochemical alterations observed under hyperglycemic conditions.

CONCLUSIONS: These data strongly support the teratogenic effect of hyperglycemia, the arachi donic acid deficiency state, the resultant maldevelopment of vitelline vessels, and the ability to prevent these changes by arachidonic acid supplementation. These studies have made significant inroads in explaining why diabetes-associated anomalies occur, and suggest a potential future role for prophylaxis against these organogenetic malformations using dietary polyunsaturated fatty acid supplementation. (J Soc Gynecol Invest 1994;1:3-13)

Key Words: Yolk sac • embryopathy • diabetes • arachidonic acid.


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