RESEARCH ARTICLE e

Full list of author information is available at the end of the articleBackground The hormone somatostatin plays a central role in the inhibition of growth hormone (GH) release from the pituitary gland [1]. Somatostatin is also secreted by gastric and pancreatic D-cells in response to meal ingestion through stimulation of the autonomic nervous system [2-4]. It suppresses the release of insulin-like growth factor-1 (IGF-1), vasoactive intestinal polypeptide, gastrin, secretin, and pancreatic polypeptides and exerts a range of physiological effects, such as modifying intestinal transit time and regulating intestinal water and electrolyte transport [1,5-8]. Somatostatin influences glucose metabolism by inhibiting insulin, glucagon secretion and IGF-1 production [9]. In type 2 diabetes mellitus (T2DM), somatostatin lowers glucose concentrations by inhibiting glucagon secretion [9,10] and abnormalities in the GH-IGF-1 axis have been associated with increased cardiovascular risk in T2DM [11-13]. The half-life of somatostatin in plasma is only 1–3 minutes and concentrations are generally in sub-picomolar amounts [14,15]. The stable precursor, the N-terminal * Correspondence