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 17 years
after preeclamptic pregnancy and may contribute to a woman's increased risk for cardiovascular
disease. Insulin resistance may not be the cause of preeclampsia, but is one of the
pathogenetic factors, especially in genetically predisposed women.
Keywords:
Insulin resistance - preeclampsia - sympathetic nervous system
