Insulin provokes co-ordinated increases in the synthesis of phosphatidylinositol, phosphatidylinositol phosphates and the phosphatidylinositol-glycan in BC3H-1 myocytes.
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.
Farese
R V
RV
James A. Haley Veterans Hospital, Tampa, FL.
Cooper
D R
DR
Konda
T S
TS
Nair
G
G
Standaert
M L
ML
Pollet
R J
RJ
D002460:Cell Line; D002855:Chromatography, Thin Layer; D005944:Glucosamine / Q000378:metabolism; D017261:Glycosylphosphatidylinositols; D007294:Inositol / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D010716:Phosphatidylinositols / Q000096:biosynthesis*; D011134:Polysaccharides / Q000096:biosynthesis; D013268:Stimulation, Chemical
D017261:Glycosylphosphatidylinositols; D007328:Insulin; D010716:Phosphatidylinositols; D011134:Polysaccharides; D007294:Inositol; D005944:Glucosamine