-transparent.png){kind=logo}
The effect of glucose on the metabolism of phospholipids in pancreatic islets was studied with three radioactive phospholipid precursors, [32P]orthophosphate, [3H]myoinositol, and [3H]arachidonic acid, to determine the conditions necessary for studying the breakdown of prelabeled phospholipids. Islets were incubated in the presence of a radioactive precursor for 60 or 90 min and in the presence of either 3.3 or 16.7 mM glucose to prelabel phospholipids. To study the breakdown of prelabeled phospholipid, the unincorporated precursor was removed and the islets were reincubated for 15 or 20 min under conditions that either did or did not stimulate insulin release. Prelabeling in the presence of a noninsulinotropic concentration of glucose (3.3 mM) supported the incorporation of precursors into almost all islet phospholipids studied. Prelabeling in an insulinotropic concentration of glucose (16.7 mM) increased the incorporation of precursors into a number of phospholipids even more; and reincubation in 16.7 mM glucose caused a rapid loss of radioactivity from specific phospholipids (phosphatidylinositol and/or phosphatidylcholine, depending on the precursor). This breakdown was observed only when islets had been prelabeled in 16.7 mM glucose. The amount of radioactivity lost from phospholipid corresponded roughly to the additional amount incorporated during the prelabeling in the high concentration of glucose. Radioactivity in phospholipids in islets prelabeled in 3.3 mM glucose or in nonsecretagogue metabolic fuels, such as malate plus pyruvate, did not decrease when the islets were subsequently exposed to 16.7 mM glucose, nor did it decrease in 3.3 mM glucose when these islets had been prelabeled in 16.7 mM glucose. Glyceraldehyde, an insulin secretagogue, but not galactose or L-glucose which are not insulin secretagogues, stimulated phospholipid breakdown in islets that had been prelabeled in 16.7 mM glucose. Depriving islets of extracellular calcium, a condition that inhibits insulin release, inhibited phospholipid breakdown. The results suggest that pancreatic islets contain a glucose-responsive and a glucose-unresponsive phospholipid pool. The glucose-responsive pool becomes labeled and undergoes rapid turnover only under stimulatory conditions and may play a role in the stimulus-secretion coupling of insulin release.
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
March 1986,
Archives of biochemistry and biophysics,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
July 1984,
Biochemical and biophysical research communications,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
October 1984,
Experientia,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
March 1984,
Biochemistry international,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
December 1976,
Science (New York, N.Y.),
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
August 1991,
Diabetes,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
September 2020,
Pflugers Archiv : European journal of physiology,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
December 1986,
Biochimica et biophysica acta,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
February 2009,
Endocrinology,
R S Rana, and
R J Mertz, and
A Kowluru, and
J F Dixon, and
L E Hokin, and
M J MacDonald
January 1986,
Journal of cellular biochemistry,
