Journal of Lipid Research, Vol 30, 1299-1305, Copyright © 1989 by Lipid Research, Inc.
Palmitic acid stimulates glucose incorporation in the adipocyte by a mechanism likely involving intracellular calcium
J Thode, HA Pershadsingh, JH Ladenson, R Hardy and JM McDonald
Department of Clinical Chemistry, Herlev University Hospital, Denmark.
The effect of palmitic acid on basal and insulin-stimulated incorporation
of glucose into rat adipocytes was studied. Palmitic acid (2.40 mM)
stimulated basal as well as insulin-stimulated glucose incorporation in rat
adipocytes three and twofold, respectively. Similar degrees of stimulation
of basal glucose oxidation by palmitate were also observed. The ability of
palmitic acid to stimulate glucose uptake was additive with respect to the
stimulation induced by insulin and was proportional to the palmitic acid
concentration between 0.15 mM and 2.40 mM. Stimulation of glucose
incorporation by palmitic acid was inhibited by preincubating the cells
with quin2-AM, which accumulates intracellularly yielding the trapped
chelator form. quin2, which binds intracellular Ca2+.The concentration of
quin2-AM required for half- maximal inhibition of palmitic acid stimulated
glucose incorporation was 3.8 +/- 1.2 microM (mean +/- SEM). The inhibition
of palmitic acid- stimulated glucose incorporation by quin2-AM (10 microM)
was overcome by incubating cells with the Ca2+ ionophore, A23187, in the
presence of extracellular Ca2+ (2.6 mM). Chelation of extracellular Ca2+
with EGTA did not significantly affect the magnitude of palmitic
acid-stimulated glucose incorporation. Dantrolene (12.5-100 microM) failed
to affect basal or palmitic acid-stimulated glucose incorporation. These
findings suggest that palmitic acid stimulates incorporation of glucose in
the adipocyte by a mechanism dependent upon intracellular but not
extracellular Ca2+.
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