AJP - Endocrinology and Metabolism, Vol 256, Issue 1 E68-E73, Copyright © 1989 by American Physiological Society
Effect of CCK-8 on pentose phosphate shunt activity, pyridine nucleotides, and glucokinase of rat islets
E. J. Verspohl, I. Breuning and H. P. Ammon
Department of Pharmacology, University of Tubingen, Federal Republic of Germany.
In rat pancreatic islets the effects of cholecystokinin octapeptide (CCK-8)
on pentose phosphate shunt (PPS) activity, glucokinase and hexokinase
activity, and NADPH, NADP+, NADH, and NAD+ were studied. By elevating the
glucose concentration from 3.0 to 8.3 and 16.7 mM the oxidation of [1-14C]-
and [6-14C]glucose and the calculated PPS activity were increased in a
concentration-dependent manner; 10 nM CCK-8 enhanced selectively the effect
on [1-14C]glucose oxidation thereby increasing the PPS activity but only at
an intermediate glucose concentration (8.3 mM). CCK-8 had no effect on
glucokinase or hexokinase activity and CCK-8 did not influence glucose
utilization. By elevating the glucose concentration, total NADPH and NADH
were increased and total NADP+ and NAD+ were decreased. CCK-8 (10 nM)
increased selectively NADPH and decreased NADP+ but did not change NADH or
NAD+; the effect of CCK-8 on NADPH and NADH was only observed in the
presence of an intermediate stimulatory glucose concentration (8.3 mM) but
not at either a substimulatory glucose concentration or a maximally
stimulatory glucose concentration for insulin release (3.0 or 16.7 mM). The
data indicate first that CCK-8 does not act on glucose phosphorylation or
glucose utilization and second that CCK-8 increases PPS activity and NADPH
levels in rat pancreatic islets. Since the concentrations of glucose
necessary for these CCK-8 effects are in the range of 8.3 mM and parallel
with those necessary for insulin release as shown in earlier observations,
glucose oxidation via pentose phosphate shunt and NADPH are suggested to be
related to the CCK-8-modulated insulin release.
