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Comparative studies of metabolism of 4‐desmethyl, 4‐monomethyl and 4,4‐dimethyl sterols in Manduca sexta
Author(s) -
Svoboda James A.,
Ross Samir A.,
Nes W. David
Publication year - 1995
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02537047
Subject(s) - lanosterol , cycloartenol , sterol , stigmasterol , ergosterol , manduca sexta , cholestanol , campesterol , biochemistry , phytosterol , metabolism , biology , chemistry , cholesterol , chromatography , botany , insect
Abstract To investigate the metabolism and possible deleterious effects of 4‐methyl and 4,4‐dimethyl steroids in Manduca sexta , the 4,4‐dimethyl sterols lanosterol and cycloartenol, the 4‐methyl sterol obtusifoliol and the 4,4‐dimethyl pentacyclic triterpenoid α‐amyrin were fed in an artificial agar‐based diet at various concentrations. Utilization and metabolism of these four compounds were compared with sitosterol, stigmasterol, brassicasterol, ergosterol and 24‐methylenecholesterol, 24‐alkyl sterols that are readily dealkylated and converted to cholesterol in Manduca and in most phytophagous insects. None of the 4‐methylated compounds significantly inhibited development except at very high dietary concentrations. The Δ 24 ‐bonds of lanosterol and cycloartenol were effectively reduced by the Manduca Δ 24 ‐sterol reductase enzyme, as is the Δ 24 ‐bond of desmosterol which, in most phytophagous insects, is an intermediate in the conversion of sitosterol, stigmasterol and other C 28 and C 29 phytosterols to cholesterol. On the other hand, the 24‐methylene substituent of obtusifoliol was not dealkylated. Each of the 4‐desmethyl C 28 and C 29 sterols was readily converted to cholesterol, and a significant amount of 7‐dehydro‐cholesterol was derived from ergosterol metabolism. The reason for the differences in substrate specificity of these sterols is not clear, but the information may be useful in the development of new, specific, mechanism‐based inhibitors of sterol metabolism.