Comprehensive Physiology Wiley Online Library

Somatostatin

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Biochemistry of Somatostatin
1.1 Structure
1.2 Biosynthesis
2 Distribution of Somatostatin in the Gastrointestinal Tract
3 Radioimmunoassay of Somatostatin in Plasma
3.1 Assay Methods
3.2 Metabolic Clearance
4 Regulation of Somatostatin Release
4.1 Release by Intraluminal Stimuli
4.2 Release by Neurotransmitters and Peptides
4.3 Intracellular Mechanisms Governing Somatostatin Secretion
5 Actions of Somatostatin in the Gut
5.1 Gastric Function
5.2 Intestinal Absorption and Secretion
5.3 Gastrointestinal Motility
5.4 Miscellaneous Effects
5.5 Somatostatin Receptors
5.6 Intracellular Mechanisms of Somatostatin Action
Figure 1. Figure 1.

Alternative mechanisms for prosomatostatin posttranslational processing.

Figure 2. Figure 2.

Immunohistochemically stained D cell in rat fundic mucosa. Cell is characterized by a long cytoplasmic process ending in a bulbous swelling, presumably at its junction with a target cell.

Courtesy of W. Weinstein
Figure 3. Figure 3.

Disappearance of somatostatin 14 (S‐14) and somatostatin 28 (S‐28) from dog plasma after 60‐min infusion of peptide at a dose of 2,000 pmol·kg−1·h−1. Plasma somatostatin‐like immunoreactivity (SLI) is expressed as percent of plateau concentration, which was obtained by averaging concentrations obtained at 45 min and 60 min of peptide infusion. Blood samples were taken at frequent intervals immediately after cessation of peptide infusion, and plasma was assayed for SLI.

From Seal et al. 223
Figure 4. Figure 4.

Effects of α‐ and β‐adrenergic blockade on epinephrine‐stimulated release of somatostatin‐like immunoreactivity (SLI) from fundic mucosal cells in primary cultures. SLI response to epinephrine (E) was studied with (open circles) and without (filled circles) background of 10 nM gastrin (G). Propranolol (0.1 and 1 μM) progressively shifted dose response to epinephrine plus gastrin to the right (open squares, triangles), whereas phentolamine (10 μM) increased response (closed triangles). Data, expressed as percentage of initial cell SLI content released, are from a single preparation and are similar to those obtained in 2 other experiments.

From Yamada et al. 283
Figure 5. Figure 5.

Intracellular mechanisms governing somatostatin release. CCK, cholecystokinin; DAG, diacylglycerol; IP3, inositol trisphosphate; PIP2, phosphatidylinositol‐4,5‐bisphosphate

Figure 6. Figure 6.

Postulated sites of action of somatostatin on its target cell: 1) inhibitory guanine nucleotide‐binding protein (Ni)‐mediated inhibition of adenylate cyclase, 2) inhibition of cAMP action, 3) Ni‐mediated inhibition of non‐cAMP‐dependent pathways, 4) dephosphorylation of receptors, 5) inhibition of cytosolic Ca2+ accumulation, 6) dephosphorylation of proteins via phosphoprotein phosphatases, and 7) inhibition of exocytosis. Ns, stimulatory guanine nucleotide‐binding protein; αs, αi, β, subunits of Ns and Ni.



Figure 1.

Alternative mechanisms for prosomatostatin posttranslational processing.



Figure 2.

Immunohistochemically stained D cell in rat fundic mucosa. Cell is characterized by a long cytoplasmic process ending in a bulbous swelling, presumably at its junction with a target cell.

Courtesy of W. Weinstein


Figure 3.

Disappearance of somatostatin 14 (S‐14) and somatostatin 28 (S‐28) from dog plasma after 60‐min infusion of peptide at a dose of 2,000 pmol·kg−1·h−1. Plasma somatostatin‐like immunoreactivity (SLI) is expressed as percent of plateau concentration, which was obtained by averaging concentrations obtained at 45 min and 60 min of peptide infusion. Blood samples were taken at frequent intervals immediately after cessation of peptide infusion, and plasma was assayed for SLI.

From Seal et al. 223


Figure 4.

Effects of α‐ and β‐adrenergic blockade on epinephrine‐stimulated release of somatostatin‐like immunoreactivity (SLI) from fundic mucosal cells in primary cultures. SLI response to epinephrine (E) was studied with (open circles) and without (filled circles) background of 10 nM gastrin (G). Propranolol (0.1 and 1 μM) progressively shifted dose response to epinephrine plus gastrin to the right (open squares, triangles), whereas phentolamine (10 μM) increased response (closed triangles). Data, expressed as percentage of initial cell SLI content released, are from a single preparation and are similar to those obtained in 2 other experiments.

From Yamada et al. 283


Figure 5.

Intracellular mechanisms governing somatostatin release. CCK, cholecystokinin; DAG, diacylglycerol; IP3, inositol trisphosphate; PIP2, phosphatidylinositol‐4,5‐bisphosphate



Figure 6.

Postulated sites of action of somatostatin on its target cell: 1) inhibitory guanine nucleotide‐binding protein (Ni)‐mediated inhibition of adenylate cyclase, 2) inhibition of cAMP action, 3) Ni‐mediated inhibition of non‐cAMP‐dependent pathways, 4) dephosphorylation of receptors, 5) inhibition of cytosolic Ca2+ accumulation, 6) dephosphorylation of proteins via phosphoprotein phosphatases, and 7) inhibition of exocytosis. Ns, stimulatory guanine nucleotide‐binding protein; αs, αi, β, subunits of Ns and Ni.

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Tadataka Yamada, Tsutomu Chiba. Somatostatin. Compr Physiol 2011, Supplement 17: Handbook of Physiology, The Gastrointestinal System, Neural and Endocrine Biology: 431-453. First published in print 1989. doi: 10.1002/cphy.cp060219