Since the discovery of somatostatin (SST) over three decades ago, its ubiquitous distribution and manifold functions are still being documented. SST is synthesized in the hypothalamus and transported to the anterior pituitary gland where it tonicaly inhibits GH and TSH secretion as well as being responsible for GH pulsatile release. Several internal feedback loops, sleep, exercise, and chemical agents control and influence SST release. SST also impacts the function of a wide variety of cells and organ systems throughout the body. Knowledge of the structures of the SSTs has resulted in recognition of the essential four core conserved residues responsible for their actions. The SSTs act through six separate SST cell surface receptors (SSTRs), members of the family of G protein-coupled receptors. Receptor ligand binding (SST/SSTR) results in cellular activities specific for each receptor, or receptor combinations, and their tissue/cell localization. Understanding the structure/function relationship of the SSTs and their receptors, including the internalization of SST/SSTR complexes, has facilitated the development of a variety of novel pharmacologic agents for the diagnosis and treatment of neuroendocrine tumors and unfolding new applications.

GH secretion is decreased in obese subjects, whereas age-adjusted IGF-I concentrations are normal. This study was undertaken to rigorously delineate the extent of obesity [elevated body mass index (BMI)] associated with decreased somatotrope secretory function resulting in apparent adult GH deficiency. The peak GH response evoked by combined arginine (0.5 g/kg infused iv over 30 min) and GHRH (1 microg/kg iv bolus) was measured in 59 healthy male subjects with BMIs ranging from normal to obese. BMI correlated with the peak evoked GH response (Pearson r = -0.59; P < 0.01), and the percentage of subjects exhibiting an abnormal evoked GH response, i.e. less than 9 ng/ml, increased from 5% for those with a BMI less than 25 (normal), to 13% for those with a BMI of 25-26.9 (mildly overweight), to 33% for those with a BMI of 27-29.9 (moderately overweight), and to 64% for those with a BMI of 30 or more (obese). BMI is a major determinant of evoked adult GH response to provocative testing. The diagnosis of adult GH deficiency using the evoked GH response in patients with even mild BMI elevation does not accurately distinguish normal from deficient responses and may result in the erroneous classification of obese subjects as GH deficient and thus unnecessarily requiring GH replacement.

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Short-term therapy with the TANTALUS System improves glucose control, induces weight loss, and improves blood pressure and lipids in obese T2DM subjects on oral antidiabetes therapy.