PRESERVATION OF GLUT-2 EXPRESSION ITS ISLET BETA-CELLS OF KILHAM RAT VIRUS (KRV)-INFECTED DIABETES-RESISTANT BB WOR RATS/

Loss of GLUT 2, the glucose transporter isoform of pancreatic beta cel ls, has been reported to accompany the onset and perhaps contribute to the pathogenesis, of insulin-dependent and non-insulin-dependent diab etes mellitus in BB/Wor and Zucker fatty rats. In this study we invest igated the effect of Kilham Rat Virus infection on GLUT 2 expression i n diabetes-resistant BB/Wor rats. Viral antibody-free diabetes-resista nt rats do not develop spontaneous diabetes, but inoculation with Kilh am Rat Virus induces autoimmune beta-cell destruction and hyperglycaem ia. Pancreas sections from normoglycaemic diabetes-resistant BB/Wor ra ts were obtained 5, 7 and 25 days after inoculation with Kilham Rat Vi rus and stained for GLUT 2 using a rabbit polyclonal antibody. At all time points, beta cells displayed GLUT 2 expression comparable to unin fected diabetes-resistant controls. Immunostained insulin content of t he beta cells also remained unchanged. Sections were also examined fro m Kilham Rat Virus inoculated diabetes-resistant rats with lymphocytic insulitis or diabetes. GLUT 2 and insulin immunostaining were unchang ed in non-diabetic rats with early insulitis. GLUT 2 beta-cell stainin g was variably reduced in diabetic rats with established insulitis and reduced beta-cell insulin immunostaining. Hence, the initial stages o f Kilham Rat Virus-induced diabetes in diabetes-resistant rats are not accompanied by a significant reduction in GLUT 2 expression. These re sults suggest that the loss of GLUT 2 does not play a significant role in the aetiology of diabetes in the Kilham Rat Virus-infected diabete s-resistant BB/Wor rat.