Diabetes, Vol 38, Issue 6 752-757, Copyright © 1989 by American Diabetes Association
Tissue-specific alterations in somatostatin mRNA accumulation in streptozocin-induced diabetes
DN Papachristou, K Pham, HH Zingg and YC Patel
Fraser Laboratories, McGill University, Montreal, Quebec, Canada.
In streptozocin-induced diabetes in rats, there is a marked increase in the
content and release of immunoreactive somatostatin (SLI) from the pancreas
and upper gut. To elucidate whether these SLI changes are associated with
alterations in somatostatin gene transcription, we measured somatostatin
mRNA (SmRNA) accumulation in these and other SLI-producing tissues.
Pancreas, stomach, jejunum, hypothalamus, and cerebral cortex were removed
from control rats, 6-wk-diabetic rats, and diabetic rats treated with
insulin for 6 wk. Total RNA was isolated by centrifugation through CsCl and
fractionated on agarose gels. A sensitive radiodensitometric hybridization
assay was used to determine SmRNA levels in absolute amounts by in vitro
synthesized sense-strand RNA as a quantitative standard and antisense cRNA
as a specific probe. SLI was determined by radioimmunoassay. SmRNA
exhibited size heterogeneity between the different control and diabetic
tissues. A 2- to 3-fold increase in total SmRNA was found in pancreas and
stomach of the diabetic rats that suppressed toward normal with insulin
treatment. These two tissues also exhibited significant 1.6- to 2.6-fold
increases in SLI, respectively. The remaining tissues showed no
diabetes-related changes in SLI or SmRNA. We conclude that in insulinopenic
diabetes, tissue SLI and SmRNA accumulation undergo parallel changes; are
increased in pancreas and upper gut, reflecting augmented somatostatin
synthesis; are reciprocally related to insulin acting directly or
indirectly on somatostatin-producing cells; and are unchanged in the lower
gut and brain, suggesting tissue-specific regulation of somatostatin gene
transcription in diabetes.