A2 Refereed review article in a scientific journal
Insulin resistance syndrome in preeclampsia
Authors: Kaaja R
Publication year: 1998
Journal: Seminars in reproductive endocrinology
Journal name in source: Seminars in reproductive endocrinology
Journal acronym: Semin Reprod Endocrinol
Volume: 16
Issue: 1
First page : 41
Last page: 6
Number of pages: 6
ISSN: 0734-8630
DOI: https://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.
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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