Insulin provokes a transient activation of phospholipase C in the rat epididymal fat pad.
Insulin is known to increase the de novo synthesis of inositol phospholipids in rat epididymal fat pads. We presently examined the effects of insulin on the hydrolysis of inositol phospholipids in this tissue. Relatively small (30-40%) but significant increases in inositol phosphates (mono-, di-, and tri-) were apparent within 30-60 s of insulin treatment in fat pads (and adipocytes); thereafter, inositol phosphates returned to control levels. These rapid insulin-induced increases in inositol phosphates appeared to be due to phospholipase C-mediated hydrolysis of inositol phospholipids, since there were associated transient decreases in these lipids during 32P pulse-chase experiments. Increases in the synthesis of inositol phospholipids were also apparent within a few minutes of insulin treatment and persisted for at least 2 h. We conclude that, in the rat epididymal fat pad, insulin has two phospholipid effects, viz. a transient activation of phospholipase C, and a persistent increase in de novo phospholipid synthesis.
D000273:Adipose Tissue / Q000201:enzymology*; D000818:Animals; D004789:Enzyme Activation; D004822:Epididymis; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D008297:Male; D010710:Phosphates / Q000378:metabolism; D010716:Phosphatidylinositols / Q000096:biosynthesis; D010761:Phosphorus Radioisotopes; D051381:Rats; D014316:Tritium / Q000378:metabolism; D010738:Type C Phospholipases / Q000378:metabolism*
D007328:Insulin; D010710:Phosphates; D010716:Phosphatidylinositols; D010761:Phosphorus Radioisotopes; D014316:Tritium; D010738:Type C Phospholipases