Evidence for participation of cytochrome b5 in microsomal Δ-6 desaturation of fatty acids

Adipose fatty acid composition in a case of generalized deficiency of cytochrome b5 reductase in congenital methemoglobinemia with mental retardation.

“…Oshino et al (1971) have detected cytochrome b5 reductase not only in liver but also in adipose tissue microsome. Under normal conditions, linoleic acid serves as substrate for the elongation and desaturation enzymes (Lee et al 1977;Okayasu et al 1977;Stegink et al 1977). Since cytochrome b5 reductase is involved in desaturation of fatty acid (Ozols 1976), generalized deficiency of this enzyme might have caused the reduction of unsaturated fatty acid synthesis.…”

Comparative in vivo and in vitro Study of the Influence of Experimental Diabetes on Rat Liver Linoleic Acid Δ6- and Δ5-Desaturation

“…The inhibition ratio of A6-desaturation is strongly decreased in severe streptozotocin diabetes [42]; this desaturation is less dis turbed in marginal diabetes. The presence of lipids in commercial diets (table III) induces a decrease in A6-desaturation, a phenome non already observed for A9- [29] and A6-desaturation [1, 5, 6, 8, 10-12, 15, 27, 29, 31, 34-36, 40], The interpretation of these re sults is complicated in vivo owing to the increase of the ß-oxidation rate that ob viously occurs in diabetic rats. If we consider the radioactivity recovered in linoleic acid (table II), there is a highly significant differ ence between the values corresponding to di abetic and control rats.…”

“…We know [19] that insu lin injection for at least 24 h to alloxan-dia betic rats restores palmitic and stearic acid desaturation; the restoration rate and its du ration depend on the dose of insulin in jected [20], the in vitro administration being ineffective [19]. After 48 h, insulin also cor rects partial inhibition of linoleic acid A6-desaturation induced by alloxan diabetes [29], Mercuri et al [31] demonstrated that insulin-induced restoration of desaturation activities is better for palmitic and stearic acid than for linoleic and a-linolenic acid. According to Peluffo et al [41], restoration of linoleic acid desaturation to normal values is not proportional to insulin dose; hypogly cemic injection of insulin does not increase this A6-desaturation.…”

“…According to Peluffo et al [41], restoration of linoleic acid desaturation to normal values is not proportional to insulin dose; hypogly cemic injection of insulin does not increase this A6-desaturation. The effect of insulin on A6-desaturation is restricted to the terminal desaturase enzyme of electron carrier bonds involved in fatty acid microsomal desatura tion [29], According to Eck et al [16], the same quantities of insulin and the same pro cessing time are necessary to restore the A6-and A9-desaturation induced by streptozotocin diabetes. Faas and Carter [17] bring to light, under certain conditions, a 'super' re pair of these desaturations, A6-desaturation being, however, more responsive to insulin than A9-desaturation.…”

Primary Structure of Cytochrome b5 from Cauliflower (Brassica oleracea L.) Deduced from Peptide and cDNA Sequences

“…In animals, the protein has been implicated as an intermediate electron donor in fatty acid desaturation (9,21), Cyt P-450 monooxygenase activity (13), cholesterol biosynthesis (16), fatty acid elongation (8), and plasmalogen biosynthesis (15). In higher plants, Cyt b5 has recently been shown to function as an intermediate electron donor in the desaturation of fatty acids (7,20) and has been suggested as a possible participant in ,B-oxidation in glyoxysomes (3).…”