Cellular bases for the lipid-related aspects of preeclampsia.
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.
Coffey
Charles G
CG
Golconda, Illinois, USA.
D005234:Fatty Liver / Q000150:complications; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications*; D011225:Pre-Eclampsia / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications