Inhibition of fatty acid synthesis prevents the incorporation of aldosterone-induced proteins into membranes.
2-Methyl-2-[p-(1,2,3,4-tetrahydro-1-naphthyl)phenoxy]propionic acid (TPIA), an acetyl coenzyme A carboxylase inhibitor, blocks the aldosterone-induced increase in transepithelial sodium transport. To examine the requirement for ongoing fatty acid synthesis and/or elongation in the aldosterone-induced alteration of cellular protein metabolism in the toad's urinary bladder, the effect of TPIA has been examined in double-labeled amino acid incorporation experiments. TPIA itself has no effect on the pattern of protein labeling in either the "soluble" or a plasma membrane-enriched fraction. However, inhibition of fatty acid synthesis selectively inhibits the aldosterone-induced incorporation of membrane proteins without altering the labeling of soluble cell protein. These results indicate that ongoing fatty acid synthesis is required for the hormone-induced changes in plasma membrane protein metabolism.
D000450:Aldosterone / Q000494:pharmacology*; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002024:Bufo marinus; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D005227:Fatty Acids / Q000096:biosynthesis*; D005260:Female; D008565:Membrane Proteins / Q000096:biosynthesis*; D009255:Nafenopin / Q000494:pharmacology*; D011422:Propionates / Q000494:pharmacology*; D001743:Urinary Bladder / Q000378:metabolism*
D000596:Amino Acids; D005227:Fatty Acids; D008565:Membrane Proteins; D011422:Propionates; D009255:Nafenopin; D000450:Aldosterone