Refereed review article in scientific journal (A2)

Insulin resistance syndrome in preeclampsia




List of AuthorsKaaja R

Publication year1998

JournalSeminars in reproductive endocrinology

Journal name in sourceSeminars in reproductive endocrinology

Journal acronymSemin Reprod Endocrinol

Volume number16

Issue number1

Start page41

End page6

Number of pages6

ISSN0734-8630

DOIhttp://dx.doi.org/10.1055/s-2007-1016251


Abstract
Because changes in lipids, lipoprotein, and other metabolic processes, such as hyperinsulinemia and hyperuricemia, found in preeclampsia resemble the main features of the insulin resistance syndrome, it has been proposed that insulin resistance may be the common denominator for such metabolic changes. Several groups, using euglycemic-hyperinsulinemic clamping or intravenous glucose tolerance tests (Bergman's minimal model technique), have demonstrated insulin resistance during late pregnancy. Women with preeclampsia had higher fasting insulin levels, but also exaggerated hyperinsulinemia, in response to an oral glucose tolerance test, which is consistent with increased insulin resistance in preeclampsia. No direct measurement of insulin sensitivity (clamp or minimal model) has as yet been performed during preeclampsia. Increased insulin resistance can activate the sympathetic nervous system and lead to an increase in expression of receptors for endothelin, both of which events lead to increased blood pressure. Hyperinsulinemia can also induce hypertriglyceridemia, leading to endothelial dysfunction and reduction of prostacyclin production. This hyperinsulinemia can persist for as long as 17 years after preeclamptic pregnancy and may contribute to a woman's increased risk of cardiovascular disease. Insulin resistance may not be the cause of preeclampsia, but is one of the pathogenic factors, especially in genetically predisposed women.


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