skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Abnormalities in glucose-stimulated insulin release, /sup 45/Ca uptake, and /sup 86/Rb efflux in diabetic Chinese hamster islets

Journal Article · · Diabetes; (United States)
OSTI ID:6472551

We loaded islets from normal and diabetic Chinese hamsters with /sup 86/Rb (an analogue for K+) and measured /sup 86/Rb efflux during stimulation with 20 mM D-glucose. Genetically diabetic Chinese hamsters were selected from a subline (L) known for subnormal pancreatic insulin release and excessive pancreatic glucagon release in vitro. /sup 86/Rb accumulation in 1 mM glucose was normal in the diabetic islets. Similar to the pattern of /sup 86/Rb efflux previously seen from normal rat and mouse islets, 20 mM glucose suppressed /sup 86/Rb efflux within 1-2 min, and efflux remained suppressed until return to 1 mM glucose in both normal and diabetic hamster islets. After the first 2 min of 20 mM glucose, suppression of /sup 86/Rb efflux was somewhat greater in the diabetic hamster islets than in the normals. In addition, glucose-stimulated insulin release and /sup 45/Ca uptake were significantly reduced in the diabetic islets. Therefore, in the diabetic hamster islets, there is at least no impairment in the initial suppression of /sup 86/Rb efflux by glucose. This suggests that the diabetic beta-cells recognize glucose and carry out the initial steps in the stimulus-secretion coupling sequence normally. The later, excessive suppression of /sup 86/Rb efflux may be due to impaired Ca/sup 2 +/-induced changes in /sup 86/Rb efflux, suggesting that defective regulation of intracellular Ca/sup 2 +/ activity, rather than defective regulation of K+ permeability, may lead to the impaired insulin secretion.

Research Organization:
Univ. of Umea, Sweden
OSTI ID:
6472551
Journal Information:
Diabetes; (United States), Vol. 5
Country of Publication:
United States
Language:
English