Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1994 Jul 13;136(1):23-8.
doi: 10.1007/BF00931600.

Insulin stimulates turnover of phosphatidylcholine in rat adipocytes

Affiliations

Insulin stimulates turnover of phosphatidylcholine in rat adipocytes

S L Macaulay et al. Mol Cell Biochem. .

Abstract

The present study investigated the effect of insulin on phosphatidylcholine turnover in rat adipocytes labelled to equilibrium with [14C]-choline. Insulin induced a rapid turnover of this major phospholipid that was maximal by 1 min and transient in nature. Following a 1 min stimulation of the cells with insulin at a maximally effective concentration (7 nM), a 4-6% decrease in the percentage of total cellular choline associated with this phospholipid was observed. This reflected a significant transient increase in the percentage of total cellular choline associated with phosphorylcholine, which together with diacylglycerol are the phospholipase C cleavage products of phosphatidylcholine. These effects were observed over a physiological range of insulin concentrations. No effect of insulin on any other choline phospholipid or metabolite (sphingomyelin, lysophophatidylcholine, glycerophosphocholine or choline) was seen. These results suggest that insulin stimulates a phospholipase C-mediated turnover of phosphatidylcholine in rat adipocytes. The rapid nature of this turnover suggests a potential role in signal transduction.

PubMed Disclaimer

Similar articles

References

    1. Biochem Soc Trans. 1989 Apr;17(2):259-68 - PubMed
    1. Endocrinology. 1987 May;120(5):2192-4 - PubMed
    1. Science. 1984 Sep 21;225(4668):1365-70 - PubMed
    1. Biochem J. 1988 Nov 15;256(1):185-8 - PubMed
    1. J Biol Chem. 1988 Mar 15;263(8):3600-9 - PubMed

Publication types

LinkOut - more resources