On the mechanism of hypocholesterolemic action of amphotericin B in rat.
The transient hypocholesterolemia phenomenon observed in rats, injected i.v. with amphotericin B (1.5 mg/kg/day) for three weeks, was investigated by in vitro [14C] acetate incorporation into the liver cholesterol. The incorporation of acetate in liver slices of treated animals increased more than two-fold (p less than 0.02) when compared with controls.When amphotericin B was added in vitro to liver slices of control rats, the incorporation of acetate into cholesterol decreased to about 65% of that observed with the corresponding controls (p less than 0.01). The results are consistent with the hypothesis that initially amphotericin B causes inhibition of de novo cholesterol synthesis resulting in hypocholesterolemia which disappears on continued treatment possibly due to compensatory increased rate of cholesterol biosynthesis.
D000666:Amphotericin B / Q000494:pharmacology*; D000818:Animals; D002784:Cholesterol / Q000096:biosynthesis / Q000097:blood*; D003864:Depression, Chemical; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism; D008297:Male; D051381:Rats; D013997:Time Factors
D000666:Amphotericin B; D002784:Cholesterol