These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Stimulation of glycolysis as an activation signal in rat peritoneal macrophages. Effect of glucocorticoids on this process.
    Author: Bustos R, Sobrino F.
    Journal: Biochem J; 1992 Feb 15; 282 ( Pt 1)(Pt 1):299-303. PubMed ID: 1311557.
    Abstract:
    1. Peritoneal macrophages were prepared from control, Escherichia coli-treated and triamcinolone acetonide-treated rats. Control and E. coli-treated rats produced resident and activated macrophages respectively. Glycolysis in these cells was studied by the fructose 2,6-bisphosphate (Fru-2,6-P2) content, lactate release and 6-phosphofructo-1-kinase (PFK-1) and 6-phosphofructo-2-kinase (PFK-2) activities. 2. In activated macrophages, lactate release and Fru-2,6-P2 content were increased several-fold compared with those in resident cells. Moreover, the response of these parameters to phorbol 12-myristate 13-acetate in activated macrophages was greater than for resident cells. 3. PFK-2 activity was moderately increased (about 3-fold), but PFK-1 activity was increased 5-fold in activated macrophages compared with resident cells. Partially purified preparations of PFK-1 were sensitive to Fru-2,6-P2, with K0.5 about 0.25 microM in both control and activated cells. However, the Vmax. of PFK-1 from activated cells was increased. In addition, AMP stimulated PFK-1, but the kinetic pattern was different from that described for Fru-2,6-P2. Moreover there was no difference in the stimulation by AMP of PFK-1 from resident and activated cells. 4. Fru-2,6-P2 content and lactate release in macrophages from triamcinolone acetonide-treated rats were decreased in both resident and activated cells. Also, the glucocorticoid inhibited PFK-1 and PFK-2 activities in both resident and activated macrophages. PFK-1 from triamcinolone acetonide-treated rats was not stimulated by Fru-2,6-P2, whereas the effect of AMP was unchanged. The effects of glucocorticoid seem to be specific for phagocytic cells, since the glucocorticoid treatment increased PFK-1 and PFK-2 activities in liver.
    [Abstract] [Full Text] [Related] [New Search]