Evidence that increased glucose cycling in islets of diabetic ob/
ob mice is a primary feature of the disease.
Efendic, Akhtar Khan Suad.
Department of Molecular Medicine. Karolinska Hospital, S-171 76
Stockholm, Sweden
APStracts 2:0106E, 1995.
Glucose cycling (GC) is increased in pancreatic islets from
hyperglycemic 6-month old ob/ob mice. We determined whether
normalization of glycemia alters islet GC and insulin release in
response to glucose as well as oxidation and utilization of the
glucose. Mice were treated with phlorizin in DMSO for 10 days which
resulted in normalization of blood glucose concentrations. Controls
received DMS0. The mice were fasted overnight, killed and their
islets isolated for measurements of insulin release at 5.5mM and
16.7mM glucose and at 16.7mM glucose plus 10mM arginine. GC was
measured by the incorporation of 3H from 3H20 into carbon-2 of
glucose, glucose oxidation by the yield of 14C02 from [U-14C]glucose
and glucose utilization by the yield of 3H20 from [5-3H]glucose.
Phlorizin treatment did not alter the response of insulin to glucose
and to glucose plus arginine. GC was 30% in the control and phlorizin
treated animals. Glucose oxidation and utilization were also the same
in both groups. In fed, 10-12 month old, mice exhibiting a broad
range of blood glucose levels, there was no correlation between GC
and either insulin release or glucose concentrations. Thus, the
islets of ob/ob mice exhibit an increased rate of GC irrespective of
glycemia. This indicates that the increased rate of GC is an
important characteristic of the diabetic syndrome in these animals
and not simply secondary to hyperglycemia.
Received 24 March 1995; accepted in final form 10 May 1995.
APS Manuscript Number E138-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 26 May 1995.