Circulating forms of somatostatinlike immunoreactivity in human plasma.

Circulating forms of somatostatinlike immunoreactivity (SLI) in humans were characterized using several chromatographic techniques. After gelfiltration chromatography on Bio-Gel P-6 columns greater than 90% of circulating SLI was of high molecular weight (MW) and eluted in the void volume. When plasma samples were passed through protein A-Sepharose columns, more than 85% of the high MW SLI was removed, indicating that this form of plasma SLI is mainly due to cross-reacting immunoglobulins. Extraction of 10-ml plasma samples from normal subjects on octadecyl silyl silica cartridges eliminated the high MW material. In addition, this extraction technique concentrated the two lower MW forms of SLI, which coelute on gel filtration chromatography with somatostatin-28 (S-28) and the tetradecapeptide form of somatostatin (S-14), respectively. Extracted plasma SLI was further analyzed by high-pressure liquid chromatography (HPLC). The results confirmed the identity of S-28 and demonstrated that S-14 is converted, in part, to Des-Alasomatostatin (S-13) following secretion into the circulation. At least four forms of SLI are thus present in human plasma: cross-reacting immunoglobulins, S-28, S-14, and S-13. Concentrations of SLI forms in the plasma of normal controls and patients with renal failure or cirrhosis were measured to assess the role of circulating somatostatin in health and disease. High MW SLI was elevated above normal in the plasma of patients with cirrhosis, but was not significantly elevated in patients with chronic renal failure. On the other hand, concentrations of plasma S-28 and S-13/14 (total concentrations of S-13 plus S-14) were elevated in patients with either chronic renal failure or cirrhosis.

[1]  M. Feldman,et al.  Role of circulating somatostatin in regulation of gastric acid secretion, gastrin release, and islet cell function. Studies in healthy subjects and duodenal ulcer patients. , 1984, The Journal of clinical investigation.

[2]  K. Alberti,et al.  Unimpaired clearance of somatostatin-14 in chronic renal failure. , 1984, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.

[3]  S. Shoelson,et al.  Familial hyperproinsulinemia. Two cohorts secreting indistinguishable type II intermediates of proinsulin conversion. , 1984, The Journal of clinical investigation.

[4]  R. Gomis,et al.  Splanchnic and Hepatic Metabolism of Somatostatin: A Study in Cirrhotic Patients with a Portacaval Shunt , 2007, Hepatology.

[5]  K. Polonsky,et al.  Plasma somatostatin 28 increases in response to feeding in man. , 1983, The Journal of clinical investigation.

[6]  T. Sanke,et al.  Three mutant insulins in man , 1983, Nature.

[7]  D. Yamashiro,et al.  Structure-activity relationships of somatostatin analogs in the rabbit ileum and the rat colon. , 1983, The Journal of clinical investigation.

[8]  A. Grubb,et al.  Interference of immunoglobulins in two glucagon radioimmunoassays. , 1982, Clinical chemistry.

[9]  K. Polonsky,et al.  Evidence for the Presence of Somatostatin 28 in Plasma , 1982, Diabetes.

[10]  J. Wass,et al.  Response of circulating immunoreactive somatostatin to nutritional stimuli in normal subjects , 1981 .

[11]  J. Gerich,et al.  Radioimmunoassay of Human Plasma Somatostatin , 1981, Diabetes.

[12]  T. Wheatley,et al.  A sensitive radioimmunoassay for immunoreactive somatostatin in extracted plasma: measurement and characterization of portal and peripheral plasma in the rat. , 1980, Endocrinology.

[13]  R Guillemin,et al.  High-molecular-weight immunoreactive beta-endorphin in extracts of human placenta is a fragment of immunoglobulin G. , 1980, Science.

[14]  M. Berelowitz,et al.  Metabolic clearance and plasma half-disappearance time of exogenous somatostatin in man. , 1979, The Journal of clinical endocrinology and metabolism.