Accordingly, it has been hypothesized that the blunted counterregulatory response in diabetes results, at least in part, from impaired intracellular communication within the islet, including excess SST signaling, which suppresses glucagon release (19), and that SSTR2 antagonist (SSTR2a) administration can ameliorate this imbalance (20-22). This evidence concerns the gene SST and diabetes mellitus.