Cellular bases for the lipid-related aspects of preeclampsia.

Abstract

Lipid accumulation - in hepatoytes (both subclinically and in acute fatty liver of pregnancy), in the endothelium of placental vessels ("acute atherosis"), and in the bloodstream - has been well established to be a consequence of preeclampsia. Hyperlipidemia (specifically hypertriglyceridemia) has been demonstrated to be a risk factor for the development of preeclampsia. These lipid-related aspects of preeclampsia may appear unrelated, but all are here demonstrated to provide evidence for a causative role for endothelin in the etiology of preeclampsia. Evidence for the potential of endothelin to cause lipid accumulation in hepatocytes and in endothelial cells, by means of activating G protein cascades in these cells, is presented. The capacity of typical free fatty acid constituents of triglycerides to "drive" interacellular G protein cascade-related events is also discussed - which, in this scheme, offers a plausible explanation for hypertriglyceridemia's role as a risk factor for developing preeclampsia. Additional evidence is provided which substantiates endothelin's capacity to cause most of the observed aberrations known to occur in preeclampsia.

• Authors: Charles G Coffey
• Journal: Medical hypotheses (Med Hypotheses) Vol. 60 Issue 5 Pg. 716-9 (May 2003) ISSN: 0306-9877 [Print] United States
• PMID: 12710909 (Publication Type: Journal Article)

Topics

• Fatty Liver (complications)
• Female
• Humans
• Hyperlipidemias (complications)
• Pre-Eclampsia (etiology, metabolism)
• Pregnancy
• Pregnancy Complications