Insulin provokes co-ordinated increases in the synthesis of phosphatidylinositol, phosphatidylinositol phosphates and the phosphatidylinositol-glycan in BC3H-1 myocytes

• Published in: Biochemical journal Vol. 256; no. 1; pp. 185 - 188
• Main Authors: Farese, R V, Cooper, D R, Konda, T S, Nair, G, Standaert, M L, Pollet, R J
• Format: Journal Article
• Language: English
• Published: England 15.11.1988
• Subjects: Cell Line; Chromatography, Thin Layer; Glucosamine - metabolism; Glycosylphosphatidylinositols; Inositol - metabolism; Insulin - pharmacology; Muscles - drug effects; Muscles - metabolism; phosphatidylinositol; Phosphatidylinositols - biosynthesis; Polysaccharides - biosynthesis; skeletal muscle; Stimulation, Chemical
• ISSN: 0264-6021; 1470-8728
• DOI: 10.1042/bj2560185

BC3H-1 myocytes were cultured in the presence of [3H]inositol or [3H]glucosamine during their entire growth cycle to ensure that all lipids containing inositol and glucosamine were labelled to isotopic equilibrium or maximal specific radioactivity. After such labelling, a lipid (or group of lipids), which was labelled with both inositol and glucosamine, was observed to migrate between phosphatidylinositol 4-phosphate and phosphatidylinositol (PI) in two different t.l.c. systems. Insulin provoked rapid, sizeable, increases in the inositol-labelling of this lipid (presumably a PI-glycan), and these increases were similar to those observed in PI and PI phosphates. Our results indicate that insulin provokes co-ordinated increases in the net synthesis de novo of PI and its derivatives, PI phosphates and the PI-glycan, in BC3H-1 myocytes. This increase in synthesis of PI may serve as the mechanism for replenishing the PI-glycan during stimulation of its hydrolysis by insulin. Moreover, increases in the content of the PI-glycan may contribute to increases in the generation of head-group 'mediators' during insulin action.