Testicular Sterols. IV. End-Product Steroid Inhibition of Lanosterol Demethylation^*

Alzheimer's Disease: Brain Desmosterol Levels

“…In this study it was noted that “steroids may preferentially inhibit cholesterol synthesis after mevalonate formation at the step between lanosterol and cholesterol.” Of the eight steroid hormones studied, progesterone had the greatest effect, which supported previous findings that demonstrated its direct effect on enzymes regulating the lanosterol-to-cholesterol metabolic pathway [31]. More recently, it was shown that progesterone, pregnenolone, and 17αOH-progesterone are potent inhibitors of ∆24-reduction, which leads to the accumulation of desmosterol [32].…”

Sterol Biosynthesis in the Bovine Corpus Luteum in Vitro*

“…On the basis of (a) the above findings in testis, (b) the accumulation of newly formed squalene in corpus luteum previously noted, and (c) the appreciable concentrations of endogenous squalene and lanosterol in this tissue, one might speculate that in both testis and corpus luteum these precursors may act as reserves for rapidly replenishing a small "steroidogenic" cholesterol pool. The recent work of Gaylor and his associates (Gaylor and Tsai, 1964;Ying et al, 1965;Gaylor et al, 1965) on control of lanosterol demethylation in testis tissue is in accord with this concept.…”

Membrane-Bound Enzymes of Cholesterol Synthesis from Lanosterol

“…From early stages of these studies we rationalized that the end product steroid in the pathway may affect metabolism of lanosterol, 1, the first steroid (45). Furthermore, the steroid could be tissue specific with bile acids acting in liver (55) and steroid hormones in testis and other hormone-secreting cells (56,57). Our first evidence in support of regulation directly by cholesterol, i.e., the end product of the 1-19 pathway, was the observation that dietary cholesterol reduced lanosterol demethylase activity to about 15% of control rats (14).…”