Plasma somatostatin 28 increases in response to feeding in man.

Abstract

A B S T R A C T Tissue somatostatin-like immunoreactivity (SLI) consists of a number of molecular species including the cyclic tetradecapeptide or SRIF, an Nterminally extended form of SRIF termed somatostatin-28, as well as larger precursor peptides. The function and nature of circulating SLI is not well understood. In this report, we describe techniques for the definition of the components of plasma SLI in normal human plasma. Plasma SLI measured after gel filtration on Bio-gel P-6 columns was found to consist of from 1-3 peaks. The void volume peak was present in greatest concentration (34.2±8.9 pg/ml) and did not increase in response to a mixed meal. Very low levels of two additional peaks of SLI activity were found. To further characterize these peaks, 10-ml plasma samples were extracted and concentrated on octadecylsilyl silica (C-18) cartridges with subsequent fractionation on Bio-gel P-6 columns. The two peaks that coeluted with synthetic SRIF and S-28 markers, respectively, were present in concentrations of 5.4±1.4 and 4.8±1.9 pg/ml in fasting plasma. In response to a mixed meal, the SLI14 peak doubled (12.9±2.4 pg/ml) while the SLI28 peak increased to 29.9±7.2 pg/ml at 120 min. These results provide evidence that S-28 circulates in human plasma and its increase after feeding is consistent with a possible biological role for this peptide.

Role of circulating somatostatin in regulation of gastric acid secretion, gastrin release, and islet cell function. Studies in healthy subjects and duodenal ulcer patients.

“…Basal plasma gastrin averaged 49±6 pg/ml in normal subjects and 93±9 pg/ml in DU patients (P < 0.05). vious reports (3)(4)(5)(6)(7)(8), although our results differ quantitatively from some of these reports. In our study, basal SLI concentrations averaged 7-9 pg/ml in healthy subjects and DU patients, whereas others have reported mean basal SLI concentrations as low as 9 pg/ml (3) or as high as 174 pg/ml (4).…”

“…Thus, it is likely that the 8 pg/ml increase in plasma SLI after the steak meal represented only S-14 somatostatin and not another species of somatostatin. Some groups using different antibodies have reported increases in S-28 in plasma after meals (6,8), whereas our group was unable to detect S-28 in canine plasma using antibody RIOI obtained from Arimura (23). It is possible that the magnitude of the total somatostatin response to a meal (S-14 plus S-28) may be even greater than estimated by antibody 80 C in the present study.…”

“…Sensitive radioimmunoassays have documented increases in circulating somatostatin-like immunoreactivity (SLI)' after meals in humans (3)(4)(5)(6)(7)(8). Although high intravenous doses of somatostatin can inhibit gastric acid secretion and gastrin release (9)(10)(11)(12), it is unknown whether the amount of somatostatin released into the circulation after a meal is of sufficient magnitude to affect gastric acid secretion or gastrin release.…”

Selective binding of somatostatin-14 and somatostatin-28 to islet cells revealed by quantitative electron microscopic autoradiography.

“…On the other hand, these sites may interact with extra islet S-28 delivered via the circulation. The largest collection of S-28-producing cells in the body resides in the gut from where S-28 is preferentially released into the blood stream postprandially (8,12,24). It is conceivable that these postprandial surges of circulating S-28 of gut origin modulate, via an endocrine mechanism, the insulin response of the meal-stimulated B cell.…”

Inhibitory effect of somatostatin on insulin secretion is not mediated via the CNS

“…SST exists as two biologically active forms, SST14 and SST28, which are derived by post-translational cleavage of a single prohormone. SST14 is expressed in neurones and most other SST-producing peripheral tissues, including d-cells, while SST28 is primarily found at high levels in the gastrointestinal tract (Low 2004), and is the major form of circulating SST (Polonsky et al 1983). The peptide often acts as an inhibitory regulator of endocrine systems, for example, as a hypothalamic factor to suppress growth hormone secretion, or as a local inhibitor of the release of gastrointestinal peptide hormones.…”